Neuronal Emotion 1

Physics of Life Reviews 4 (2007) 37–63
www.elsevier.com/locate/plrev
Review
Neural network modeling of emotion

Daniel S. Levine ∗
Department of Psychology, University of Texas at Arlington, 501 S. Nedderman Drive, Arlington, TX 76019, USA
Received 6 July 2006; accepted 9 October 2006
Available online 15 November 2006
Communicated by L. Perlovsky
Abstract
This article reviews the history and development of computational neural network modeling of cognitive and behavioral
processes that involve emotion. The exposition starts with models of classical conditioning dating from the early 1970s. Then
it proceeds toward models of interactions between emotion and attention. Then models of emotional influences on decision making
are reviewed, including some speculative (not and not yet simulated) models of the evolution of decision rules. Through the late
1980s, the neural networks developed to model emotional processes were mainly embodiments of significant functional principles
motivated by psychological data. In the last two decades, network models of these processes have become much more detailed
in their incorporation of known physiological properties of specific brain regions, while preserving many of the psychological
principles from the earlier models.
Most network models of emotional processes so far have dealt with positive and negative emotion in general, rather than specific
emotions such as fear, joy, sadness, and anger. But a later section of this article reviews a few models relevant to specific emotions:
one family of models of auditory fear conditioning in rats, and one model of induced pleasure enhancing creativity in humans. Then
models of emotional disorders are reviewed. The article concludes with philosophical statements about the essential contributions
of emotion to intelligent behavior and the importance of quantitative theories and models to the interdisciplinary enterprise of
understanding the interactions of emotion, cognition, and behavior.
© 2006 Elsevier B.V. All rights reserved.
Keywords: Neural networks; Emotion; Cognition; Behavior; Dynamical systems
Contents
1. Introduction: the uses of emotion and affect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

2. Early models of Pavlovian conditioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40
2.1. Theoretical foundations of neural networks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 40
2.2. Associative learning models in conditioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 41
2.3. Modeling context and affective valence: gated dipoles and temporal difference . . . . . . . . . . . . . . . . . . . . . . . 43
3. Models of emotional influences on attention . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
4. Models of emotionally influenced decision making . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48
* Tel.: +1 817 272 3598; fax: +1 817 272 2364.

E-mail address: levine@uta.edu (D.S. Levine).
1571-0645/$ – see front matter © 2006 Elsevier B.V. All rights reserved.
doi:10.1016/j.plrev.2006.10.001
38 D.S. Levine / Physics of Life Reviews 4 (2007) 37–63
4.1. Individual decision making under risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

4.2. Social influences and long-term behavioral development . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 50
5. Models of specific emotions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
5.1. Models of fear conditioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
5.2. A model of positive affect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 54
6. Models of emotional disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
6.1. Overarousal and underarousal, schizophrenia, and autism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 56
6.2. Excitatory-inhibitory imbalance, manic-depression, and unipolar depression . . . . . . . . . . . . . . . . . . . . . . . . . 56
7. Concluding remarks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
Acknowledgement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
Appendix A. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 58
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 60
1. Introduction: the uses of emotion and affect
The scientific study of emotion has been in the ascendancy since about the early 1990s. Before that time, the com-
puter information processing metaphor that drove both cognitive psychology and artificial intelligence in the 1960s
and 1970s tended to reduce emotion to second-class status in those intellectual communities. Yet as more knowledge
emerged from cognitive and behavioral neuroscience, it gradually became apparent that cognitive processes such as
attention, memory, categorization, language understanding, and decision making could not be properly understood
without including emotional influences on these processes. As this article will review, neural network models have
actually dealt with some of these influences for over 30 years—not with specific emotions such as fear, sadness,
anger, and joy, of which models are just beginning to emerge, but with generalized positive and negative affect as they
influence learning and behavior.
There is some confusion in the scientific literature between three commonly used and closely related terms: emo-
tion, affect, and mood. In clinical terminology, “emotion” tends to be used for what a person is feeling at a given
moment. Joy, sadness, anger, fear, disgust, and surprise are often considered the six most basic emotions, and other
well-known human emotions (e.g., pride, shame, regret, elation, et cetera) are often treated as elaborations or special-
izations of these six to complex social situations. “Affect” tends to be used for the outward, physical signs of emotion,
as in the phrase “flat affect” to describe the presentation of some types of schizophrenics. “Mood” tends to be used for
a pervasive emotion over a longer period of time, anywhere from a day to several years. However, psychologists and
modelers are far from consistent in their use of these terms; in particular the words “emotion” and “affect” are often
interchanged.
Many recent scholars have attempted to formulate a comprehensive definition of emotion. Yet by and large they
have not been able to improve on Aristotle’s statement (in Rhetoric) that “Emotion is that which leads one’s condition
to become so transformed that his judgment is affected, and which is accompanied by pleasure and pain”. More recent
definitions of emotion have either emphasized the external stimuli that trigger emotion [1–3] or the internal responses
involved in the emotional state [4], when in fact emotion includes both of those things and much more. Hence, my own
usage of the terms emotion and affect will not follow any strict guidelines but be flexible, to facilitate consideration
of functionally significant processes in which emotion plays a role.
There is also a long-standing dispute among experimental psychologists as to whether emotions are primarily
physiological or primarily cognitive. On the physiological side, Robert Zajonc [5] noted that emotional states are
often difficult to verbalize, that emotional experience can be induced by electrical stimulation of the brain, and that
emotions occur in infants and nonhuman animals. On the cognitive side, Richard Lazarus [6] noted that our emotional
experience of an event is heavily influenced by our appraisal of the potentially helpful or harmful effects of the
event on our well-being. Moreover, other investigators (e.g., [7]) have shown that the same physiological signs can
be associated with more than one emotion, and that the context of the emotion-inducing event can influence which
emotion is actually experienced. Since emotional experience is subjective and difficult to measure, the laboratory
evidence does not clearly point in either the “physiological” or the “cognitive” direction. As the neuroscience of
emotion has become better understood, unified treatments have emerged that incorporate both the physiological and
cognitive aspects into a system framework (e.g., [8]).
D.S. Levine / Physics of Life Reviews 4 (2007) 37–63 39
Table 1
Roles for emotion (adapted with permission from [9])
1. Emotion as a guide to information
2. Emotion as a selective attentional spotlight
3. Emotion as a motivator of behavior
4. Emotion as a common currency for comparing alternatives
Perhaps the most influential figure in the revival of scientific interest in emotion has been the clinical neuroscientist
Antonio Damasio. In his first book [9], Damasio described several of his patients who had sustained damage to a
part of the brain (the orbital and medial prefrontal cortex) that mediates emotional influences on cognition and action.
Contrary to the conventional wisdom that says “emotion and reason are opposites”, these patients were severely
impaired in their ability to organize and plan goal-directed behavior, despite many of them having high IQs and
excellent performance on cognitive problem-solving tasks.
Yet some of the ideas for which Damasio is known had actually been in circulation much longer, both in the
neuroscience and neural modeling communities. A behavioral neuroscientist writing in the 1970s, Walle Nauta [10],
ascribed to the frontal lobes (without specifying which prefrontal subregion) a function that he called interoceptive
censorship of plans. This means that each potential behavioral plan is internally “rehearsed” to see how the viscera
react to it, and if the visceral reaction is overly negative, performance of the plan is inhibited. Around the same time,
the pioneering neural network modeler Stephen Grossberg [11,12] included drive, or emotion, nodes in his early
networks to enable different sensory patterns of significance to the organism (such as those representing a source of
food and a sexual partner) to overcome mutual interference when presented close together.
From the evolutionary viewpoint, what is emotion “good for”? The psychologist Ellen Peters [13] reviewed several
separate but interacting roles that emotion plays in decisions among competing behaviors. She stated that emotion (she
called it “affect”) is, at different times, (1) a guide to information; (2) a selective attentional spotlight; (3) a motivator
of behavior; and (4) a common currency for comparing alternatives. These are listed in Table 1.
All the functions listed in Table 1 relate to satisfactions of the organism’s basic needs and therefore have clear
evolutionary value. In addition to the utility of emotion in general, there are some widely recognized evolutionary
functions of specific emotions. Robert Plutchik [14] described some functions of basic emotions as follows: for fear,
protection against threats; for anger, destruction of obstacles; for joy, facilitation of social connections and reproduc-
tion; for sadness, reintegration with significant others; for disgust, rejection of potentially harmful objects; for surprise,
orientation to one’s environment. Also, Carroll Izard [15] described the social functions of outward emotional expres-
sions, such as facilitating communication of internal states, regulating others’ responses, facilitating social interactions
and encouraging prosocial behavior.
Such functions of specific emotions, and of outward emotional expressions, are beyond the scope of current neural
network models but seem likely to become the subject of future neural network models. Since these future models are
likely to build on existing neural network models of simpler emotional processes and cognitive-emotional interactions,
I focus in this review on the simpler processes for which models have already been developed. Also, this review
concentrates on neural networks that model emotions in biological organisms, and does not consider neural networks
used in engineering applications for emotion recognition (e.g., [16–18]).
In the last decade, the general functions of emotion shown in Table 1 have become widely recognized not only by
cognitive neuroscientists and psychologists, but also by researchers in artificial intelligence and in various aspects of
neural engineering who have come to see emotion as a necessary component of complex intelligent functioning (e.g.,
[19]). In particular, many engineers have included analogs of generalized positive and negative emotions in the design
of robots in order to facilitate the robots’ learning of which objects to approach or avoid (e.g., [20–22]).
Role (4) of Table 1, emotion as a common currency, has played a particularly important part in recent developments
based on brain imaging studies that have shown, for example, that in humans monetary rewards often activate the same
brain regions as primary biological rewards [23]. This result has been one of many that have stimulated the burgeoning
field known as neuroeconomics (e.g., [24]).
However, in the early development of network models of emotion, its most important roles were (1) and (3) of
Table 1, emotion as a guide to information and as a motivator of behavior. Much of this work was stimulated by
theoretical approaches to conditioning from mid-twentieth century psychologists such as Clark Hull, Donald Hebb,
and Hobart Mowrer. For example, Hebb [25] noted that emotionally significant stimuli perform both a cue function
that guides behavior and an arousal function that energizes behavior, and that the two functions are somewhat separate.
We now turn to the first significant neural network models to include aspects of emotion, which were the condi-
tioning models of the 1970s and 1980s.
2. Early models of Pavlovian conditioning
2.1. Theoretical foundations of neural networks
The types of neural networks we discuss are mathematical and computer models composed of simulated brain
regions, or analogs of brain regions, and connections between them. The networks are designed with the goal of
achieving with computer simulations some results that can be interpreted as analogous to some set of behavioral or
neural or psychological data (see [26] for review). The networks discussed here are typically not three-layer feedfor-
ward networks with back propagation of weights [27], which are the most widely known type of neural networks but
actually constitute only a fraction of the neural networks in the literature.
Neural network model construction sometimes goes “top down” from observed human or animal behavior. At other
times it goes “bottom up” from the physiology of neurons comprising the brain. It can start either with psychological
data or with neurobiological data, and is then often refined to make it fit better with the other type of data. The level
of understanding that is reached is often sufficient to suggest experimental predictions at any of several levels (e.g.,
behavior—normal or pathological; single-neuron responses; neurochemistry; EEG recordings; or magnetic resonance
imaging of brain regions).
The term neural network is also used for some nonbiological networks with industrial applications, and there is not
yet a universally accepted definition that covers both the biological and nonbiological cases. Perhaps the closest is the
following [28]:
a neural network is a system composed of many simple processing elements operating in parallel whose function
is determined by network structure, connection strengths, and the processing performed at computing elements or
nodes. . . . Neural network architectures are inspired by the architecture of biological nervous systems, which use
. . . processing elements operating in parallel.
What is meant by the nodes (or elements) in this definition? Nodes are most often identified with large groups of
neurons or with brain regions, whose boundaries may not yet be precise. Sometimes, in fact, nodes are interpreted
as representations of psychological entities (stimuli, drives, etc.) whose location in the brain might or might not be
specified. However, even though nodes seldom represent individual neurons, there are many models wherein some
node activity patterns are similar to single-neuron electrical activity patterns in some brain regions relevant for the
behavior being modeled.
In the late 1960s, several modelers began to develop principles for fitting biologically relevant neural network
architectures to specific cognitive and behavioral functions. This led to models requiring partial verification on both
the physiological and the behavioral levels, and a “toolkit” of modeling techniques and modules still in wide use.
In particular, Stephen Grossberg and his colleagues (cf. [29]) developed differential equations using two sets of
variables: node activities and connection weights, which were inspired by the psychologist Clark Hull’s previous
notions of stimulus trace and associative strength [30]. For each stimulus A, the stimulus trace xA (t) measures how
active the memory for A is at any given time t. For each pair of stimuli A and B, the associational strength wAB (t)
measures how strong the sequential association AB is in the network’s memory at time t . Node activities are analogous
to short-term memory (STM) and connection weights are analogous to long-term memory (LTM). The decay rate for
LTM traces is set much smaller than the decay rates for STM traces.
An example of the equations Grossberg developed can be seen in a simple network called the outstar [31]. The
outstar was one of the first networks to learn distributed patterns, and was later used as a component in more complex
multilevel categorization networks [32]. In an outstar, one node (or vertex, or cell population) v1 , called a source,
projects to other nodes x2 , x3 , . . . , xn , called sinks, as shown in Fig. 1. The relative proportions of sink node activities
are interpreted as a spatial pattern, and Grossberg proved theorems indicating under what conditions those proportions
converge as time gets large to the pattern of inputs to those nodes. The outstar is a good illustration of the general
Fig. 1. Outstar architecture. Squares denote nodes. Semicircles denote modifiable excitatory connections. (Adapted from [33] with permission from
Elsevier Science.)
method because it is a component of larger networks designed to perform various psychological tasks, including those
involved in both classical conditioning and categorization.
For the outstar, denote the source node activity by x1 ; the sink node activities by x2 , x3 , . . . , xn ; the learnable
source-to-sink weights by w2 , w3 , . . . , wn ; the (time-varying) input to the source node by I1 ; and the (time-varying)
inputs to the sink nodes by I2 , I3 , . . . , In . Then in one version of the theory, the node activities and weights change
over time according to the following system of nonlinear differential equations:
dx1
= −ax1 + I1 ,
dt
dxi
= −axi + bx1 w1i + Ii , i = 2, . . . , n,
dt
dw1i
= x1 (−cw1i + xi ), i = 2, . . . , n, (1)
dt
where a, b, and c are positive constants and c is much smaller than a, indicating that LTM decay is much slower than
STM decay.
With this background we can proceed to discuss models of classical conditioning (also known as Pavlovian condi-
tioning), the type of learning that occurred when Ivan Pavlov trained dogs to salivate to the sound of a bell after many
pairings of the bell with food [34].
2.2. Associative learning models in conditioning
Grossberg [11,12] developed a modeling framework for classical conditioning (also, in [11], including operant
or Skinnerian conditioning, the learning of rewarded responses). His framework incorporated some of the roles for
emotion listed in Table 1. The neural network of [11] included drive nodes in addition to sensory and motor nodes.
The idea was that, for example, a dog learning to associate the sound of a bell with salivation is not learning an
association of a stimulus with a specific behavioral response, but rather a more general association of a stimulus (bell)
with satisfaction of an internal drive (hunger).
Fig. 2 shows a neural network structure for learning emotional values of one or more conditioned stimuli (CS1
and CS2 ), such as a bell or light, in the presence of an unconditioned stimulus (US), such as food or electric shock.
The network included learnable connections from the first stage of sensory nodes to drive nodes, and other learned
connections from drive nodes to a second stage of sensory nodes. The weight of a connection from a sensory to a drive
locus was interpreted as positive reinforcement for the stimulus represented by that sensory node. (This article included
only drives relating to positive emotions, whereas subsequent articles [35,36] also incorporated drives relating to
negative emotions.) The weight of the reverse connection from drive to sensory was interpreted as incentive motivation
to approach that stimulus.
Fig. 2. Network used to simulate attentional effects in Pavlovian conditioning. Each CS or US sensory representation has two stages with activities
xi1 and xi2 . Activation of xi1 generates unconditioned signals to xi2 and conditioned reinforcer signals to a drive node y. Conditioned incentive
motivational signals from y activate the second sensory stage xi2 , which sends feedback to xi1 . Arrows denote nonmodifiable excitatory connec-
tions. Semicircles denoted excitatory connections whose weights can change with learning. Filled circles denote inhibitory connections. (Adapted
from [40] with permission of the Optical Society of America.)
As more information has become available about the roles of brain areas in motivation and learning, some anatom-
ical identification of nodes in Fig. 2 has become plausible. In recent articles (e.g., [37]), the model defined by variants
of that diagram is called the CogEm model (for “cognitive-emotional”). The first sensory stage, defined by the nodes
xi1 of that figure, is identified with sensory areas of cortex. The second sensory stage, defined by the nodes xi2 , is
identified with the orbital prefrontal cortex, the part of cortex most closely connected to emotion-related regions ly-
ing below the cortex. The motivational stage, defined by the node y, is identified with the amygdala, the primary
subcortical locus for coding emotional significance and valence (positive or negative nature) of events.
The network of [12] added attention (role (2) of Table 1) to the consideration of classical conditioning. As Fig. 2
shows, the different sensory nodes also compete for attention via lateral inhibition. The simplest form of lateral
inhibition is the recurrent type in which each node excites itself and inhibits all the others equally; an example of the
equations for this inhibition among arbitrarily many nodes xi was developed and mathematically studied in [38,39]:
dxi
= −axi + (bi − xi )f (xi ) − xi f (xk ) (2)
dt
k=i
with a and b positive constants, and f a monotone increasing function such that f (0) = 0 (in simulations f is often a
sigmoid function). The term (bi − xi )f (xi ) denotes shunting self-excitation, that is, the node sends
itself an excitatory
signal proportional to the difference of its activity from a maximum value bi . The term −xi k=i f (xk ) denotes
shunting inhibition, that is, the node receives from each of the other nodes an inhibitory signal proportional to the
difference of activity from a minimum value (in this case, the minimum is 0).
Eq. (2) imply that the inputs to the nodes xi have been shut off, and that the network transforms the memory
traces of these inputs by recurrent lateral interactions. The competition between the nodes is biased by several factors
including intensity and emotional significance of the inputs the nodes represent. In the equations for the network
of Fig. 2 (which are given in Appendix A), the CS and US inputs are continuously arriving while the recurrent
interactions are taken place, yet the network dynamics are governed by the same biased competition laws that were
found by mathematical analysis of the simpler equations in [38,39].
In the competition for attention, emotionally significant sensory representations (i.e., representations of stimuli
that possess either innate or learned associations with primary drives), have a selective advantage. These include
both unconditioned stimuli and previously learned conditioned stimuli. A later article [40] carried this interplay of
association and competition into a simulation of some attentional paradigms in conditioning, such as the blocking of
formation of associations to a new stimulus if another stimulus already conditioned is also present [41].
2.3. Modeling context and affective valence: gated dipoles and temporal difference
Several early neural network models considered the effects of both reward and punishment [35,36,42,43]. Some of
them also considered the interplay of positive and negative affect via opponent processing, that is, feeling one emotion
when a source of the opposite emotion is removed [35,36]. Klopf [42] proposed that a synapse is increased in efficacy
if its activity is followed by a net increase in the depolarization (positive stimulation) received by the postsynaptic
cell. In other words, he proposed that depolarization acts as positive reinforcement for neurons. Klopf’s theory was
based on an analogy between single neurons and whole brains, both treated as goal-seeking devices. This is the reason
for the words “hedonistic neuron” in his title.
This meant that in Klopf’s theory, learning at connection weights is influenced by change in node activity, rather
than activity itself. The importance of activity change was also highlighted in Rescorla and Wagner’s quantitative
psychological theory [44], which did not arise from a neural network but has influenced the work of many neural
modelers. Their theory is based on the results of classical conditioning experiments indicating that associative learn-
ing of a conditioned stimulus can be greatly influenced by the background stimuli present during both training and
recall trials. The main tenet of Rescorla and Wagner’s theory was that “organisms only learn when events violate
expectations. Certain expectations are built up about the events following a stimulus complex: expectations initiated
by the complex and its component stimuli are then only modified when consequent events disagree with the composite
expectation” (p. 75).
Sutton and Barto [45] modeled some classical conditioning data with a theory that included elements of both
the Rescorla–Wagner and Klopf theories. Their conditioning model includes n stimulus traces xi (t), an output signal
y(t), and n connection weights wi (t), as shown in Fig. 3. These weights are considered to denote associations between
conditioned stimuli (labeled CS) and a primary reinforcer or unconditioned stimulus (labeled US). Learning is assumed
to occur at discrete time steps, leading to difference equations.
Sutton and Barto proposed that in addition to the stimulus traces which denote the duration and intensity of given
CSs, there are additional traces that are separate from the stimuli and longer lasting. These are the actual short-term
memory traces, but Sutton and Barto termed them eligibility traces because they indicate when a particular synapse
is eligible for modification. Possible cellular mechanisms were suggested for eligibility traces, involving calcium ions
and cyclic nucleotides. Finally, the current amount of reinforcement, y(t), was compared with the weighted average
of values of y over some time interval preceding t . This led to the following system of equations relating the CS
node activities xi (t), output activity y(t), CS-to-output weights wi (t), eligibilities x̄i (t), and ongoing output level
Fig. 3. Network with n learnable conditioned stimulus (CS) pathways, and a pathway with fixed weight w0 for the unconditioned stimulus (US).
The node y represents unconditioned conditioned responses (UR and CR). (Adapted from [34], copyright 1981 by the American Psychological
Association, by permission.)
ȳ(t) (representing a weighted average of past output activities):
x̄i (t + 1) = α x̄i (t) + xi (t),

ȳ(t + 1) = β ȳ(t) + (1 − β)y(t),

wi (t + 1) = wl (t) + c y(t) − ȳ(t) x̄i (t),
n

y(t) = f wj (t)xj (t) + w0 (t)x0 (t) ,
j =1
where y(t) is bounded to remain in the interval [0, 1] (that is, replaced by 1 if it gets above 1), and ß are constants
between 0 and 1; f is a sigmoid function, c is a positive constant determining the rate of learning; and x0 (t) and w0 (t)
are the activity and associative strength of the US trace.
The two innovations in Sutton and Barto’s model—eligibility traces and learning dependent on change in postsy-
naptic activity—were motivated by results on timing in classical conditioning. In particular, the model was designed
to explain the fact that in many conditioning paradigms, the optimal interstimulus interval (defined as the time delay
between CS presentation and US presentation) is greater than 0. Sutton and Barto’s network can also simulate other
contextual effects in classical conditioning, such as the blocking paradigm mentioned earlier.
Sutton and Barto’s work was elaborated by Klopf [46] and others into the differential Hebbian learning rule (also
called the drive-reinforcement rule), whereby connection weights from one node to another change as a function of
changes over time in both node activities. Klopf was led to such a rule by his earlier hedonistic neuron theory in which
neurons themselves were goal-seeking.
Klopf’s network simulated a wide variety of classical conditioning data. These data included blocking, secondary
conditioning, extinction and reacquisition of an extinguished response, conditioned inhibition, effects of interval be-
tween CS and US occurrences, effects of stimulus durations and amplitudes. However, the simulations of CS-US
interval effects depend on some weighting factors for time delays, factors that were chosen specifically to match those
data, and not generated by an underlying neural mechanism.
The learning law involving change in postsynaptic activity is not the only possible way to simulate timing effects
or blocking in classical conditioning. The same data were simulated by Grossberg and Levine [40] using a form of the
earlier Grossberg learning law based on associative learning (as in the outstar equations (1)) combined with attentional
effects, due to lateral inhibition (as in (2)), in a larger network (see Eqs. (A.1a) and (A.1h) of Appendix A).
Also, Grossberg and his colleagues have incorporated into conditioning models a mechanism for affective opponent
processing. This is the basis for an architecture called the gated dipole.
Gated dipoles were introduced by Grossberg [35,36] to answer the following question about reinforcement. Sup-
pose an animal receiving steady electric shock presses a lever which turns off the shock. Later, in the same context,
the animal’s tendency to press the lever is increased. How can a motor response associated with the absence of a
punishing stimulus (shock) become itself positively reinforcing? In other words, how does the removal of a source of
negative emotion take on a positive rather than a neutral emotional valence?
Fig. 4 shows a schematic gated dipole. The synapses w1 and w2 , marked with squares, have a chemical transmitter
that tends to be depleted with activity. The equations for changes in the connection weights w1 and w2 incorporate
what is sometimes called an anti-Hebbian learning law because the direction of change with use is opposite to the one
Hebb [47] and others use for associative learning—and which was also used in the outstar equations (1). The rate that
transmitter recovers from depletion is proportional to the difference of the amount of transmitter from its maximum
value (see Eq. (A.2) of Appendix A).
The input J in the network of Fig. 4 represents electric shock, for example. The input I is a nonspecific arousal
to both channels y1 -to-x1 -to-x3 and y2 -to-x2 -to-x4 , which compete for activation. While shock is on, the left channel
receives more input than the right channel; hence transmitter is more depleted at w1 than at w2 . But the greater input
overcomes the more depleted transmitter, so left channel activity x1 exceeds right channel activity x2 . This leads, by
feedforward competition between channels, to net positive activity from the left channel output node x3 . For a short
time after shock is removed, both channels receive equal inputs I but the right channel is less depleted of transmitter
than the left channel. Hence, right channel activity x2 now exceeds x1 , until the depleted transmitter recovers. Again,
competition leads to net positive activity from the right channel output node x4 . This right channel activity is an
Fig. 4. Schematic gated dipole network. J is a significant input (in the example of [36], electric shock) while I is nonspecific arousal. The synapses
w1 and w2 can undergo depletion (as w1 has in this diagram), as indicated by partial lightening of square boxes. After J is shut off, w1 < w2
(transiently), so x1 < x2 . By competition, x4 is activated, enhancing a motor output suppressed by J . (If the significant input J has positive affective
valence, the excitatory and inhibitory arrows going to x5 are reversed.)
Fig. 5. Typical time course of the channel outputs of a gated dipole. (Adapted from [50], with permission from Elsevier Science.)
example of an antagonistic rebound: activity of a representation of the opposite response after the original stimulus is
removed.
Whichever channel has greater activity either excites or inhibits x5 , thereby enhancing or suppressing a particular
motor response. The network is called a gated dipole because it has two channels that are opposite (“negative” and
“positive”) and that “gate” signals based on the amount of available transmitter. Characteristic output of one gated di-
pole is graphed in Fig. 5. This graph illustrates the rebound in x4 activity after the cessation of x3 activity. Grossberg’s
work was concurrent with Solomon and Corbit’s opponent processing theory of motivation [48], whereby significant
events elicit both an initial reaction and a subsequent counterreaction. Indeed, Grossberg hinted that a gated dipole
can exhibit switching back and forth between opposite responses [49].
Grossberg used this transmitter depletion mechanism to model the effects of stimulus changes rather than a simple
time difference mechanism, in order to capture two specific effects found in conditioning experiments. One is that the
positive reinforcement value of escape from shock is sensitive to both its intensity and its duration (e.g., [51]). The
other is that the amount of reinforcement depends on the overall arousal level of the network (or organism) (e.g., [52]).
If the two channels in Fig. 4 are reversed in sign so that the channel receiving input is the “positive” one, the network
provides an explanation for the negative emotion of frustration that is induced when a source of positive emotion either
is terminated, or does not arrive when expected. The rebounds between positive and negative emotions also explain
the experimental finding that motor responses that are intermittently rewarded are more resistant to extinction than are
responses that are always rewarded [53]. According to the gated dipole theory a reward’s attractiveness is enhanced
by comparison with an expected lack of reward; Section 4 of this article discusses such comparisons further in the
context of decision making models.
The interplay of positive and negative emotions was developed more fully in a subsequent article by Grossberg
and Schmajuk [54]. These authors combined the gated dipole with associative learning and reverberating loops to
enable the network to simulate both primary and secondary appetitive conditioning (learning to approach a stimulus
paired with reward such as food) and aversive conditioning (learning to avoid a stimulus paired with punishment such
as shock). Secondary conditioning means that if a conditioned stimulus CS1 (e.g., a bell) is presented prior to the
unconditioned stimulus US (e.g., food or shock) often enough to become a predictor of the US’s occurrence, then that
CS1 becomes a reinforcer in itself. Hence if another stimulus, CS2 (e.g., a light), is repeatedly presented prior to CS1 ,
an animal learns to approach or avoid CS2 , depending on whether the US is an appetitive or aversive stimulus.
The network of [54], called READ (an acronym for “recurrent associative dipole”), also simulated the positive
emotion of relief from the absence of expected punishment and the negative emotion of frustration from the absence
of expected reward. A later article by the same authors, [55], added a spectrum of nodes with different time delays, so
that the network can learn to expect rewards or punishments at the appropriate time intervals and not become frustrated
or relieved if the rewards or punishments do not arrive sooner.
Comparison of current rewards or penalties with expected ones has been accomplished by other models using a dif-
ferent construction than the gated dipole, a construction called temporal difference. Sutton and Barto [56] constructed
a variant of their 1981 model whereby connection weights change with the difference of total positive reinforcement
from total positive reinforcement at the previous time step. This included a factor whereby future reinforcement was
proportionately discounted relative to current reinforcement. The temporal difference (TD) idea was extended further
by analogies with firing patterns of dopamine neurons in the midbrain [57–59]. These dopamine neurons respond with
bursts of electrical activity to unexpected rewards, and respond with dips in activity to unexpected absences of reward.
Brown et al. [60] also modeled the dopamine cell data in the network they developed for response to unexpected
rewards. They contrasted their own model with the TD models of Schultz and his colleagues.1 They noted that the TD
models suggest that the dopamine cells compute a temporal derivative of predicted reward. They argued that putting
all the interactions at one node in the network caused some problems for reproducing the timing data. Specifically,
they argued that the Suri–Schultz model can only learn a single fixed interstimulus interval that corresponds to the
longest-duration timed signal in their model. Also, the Suri–Schultz model predicts a lasting depression of dopamine
firing subsequent to primary reward, which is not found in the data. The model of [60] avoids this difficulty by utilizing
two distinct pathways: a part of the basal ganglia and a part of the midbrain for initial excitatory reward prediction,
and a different part of the basal ganglia for timed, inhibitory reward prediction. This study indicates the potential for
neural networks to show that specific details of the anatomical and physiological structures are functionally important
for their behavioral properties.
Conditioning becomes more complex and difficult when the CS and US are separated in time. Fig. 6 shows schemat-
ically the difference between delay conditioning and trace conditioning. Delay conditioning is the standard paradigm
in which the CS is introduced before the US but there is at least some overlap between their presentation times; trace
conditioning is the paradigm in which the CS is removed before the US is introduced.2 Trace conditioning is harder
to achieve than delay conditioning, because trace conditioning requires associating one stimulus with the memory of
another stimulus that is no longer present.
We noted earlier that in recent articles (e.g., [37]), Grossberg’s conditioning system schematized in Fig. 2 has
been interpreted as including sensory cortex, amygdala, and orbital prefrontal cortex. Animal lesion data suggest that
trace conditioning, also requires regions involved in memory consolidation and timing, such as the hippocampus.
A network study in progress [61] adds a parallel hippocampal system to earlier conditioning networks [37,54] to
account for multiple time frames in conditioning data. The ensuing network simulates some data on amnesia as well
as trace conditioning.
Classical conditioning is sometimes disdained by cognitive psychologists as an overly simple form of learning.
However, understanding conditioning and animal learning properly requires consideration of attentional and timing
1 The model of [60] does not include a gated dipole. It is similar to the gated dipole model, however, in that it separates sites for appetitive and
aversive learning, unlike the TD models which place appetitive and aversive learning at the same location.
2 The term “trace conditioning” makes sense because it relates to memory traces. But the term “delay conditioning” seems to mean the opposite
of what it intuitively should mean!
Fig. 6. Delay versus trace conditioning. “ISI” refers to the interval between stimulus presentation start times.
influences, not just primitive emotional associations. Hence both for network modelers and cognitive neuroscientists,
conditioning has served as a gateway to the understanding of more advanced forms of learning and other cognitive
processes, including processes that are unique to humans. This particularly includes processes in which emotion plays
a role in selective attention or in decision making, which are covered in the next two sections.
3. Models of emotional influences on attention
Recent brain imaging and evoked potential studies have shed further light on the neural bases for the different roles
of emotion. In particular, there are many results on how the amygdala and different parts of the cortex and thalamus
process emotional versus nonemotional stimuli. These results have uncovered subtle interactions between emotion and
cognitive processes such as attention (role (2) of Table 1). Such emotional-attentional interactions have been modeled
by variations on neural networks previously developed for attentional processes in the absence of emotion (e.g., [62]).
Emotional stimuli are traditionally thought to engage a more primitive form of processing, involving the amygdala
along with other subcortical brain areas such as the hypothalamus, the gateway to the viscera. Therefore, the reaction
to emotional stimuli has been regarded as automatic and not requiring attention. Yet the brain imaging results of
Pessoa et al. [63] (see also [64]) challenged this traditional view of emotional automatism. Pessoa and his colleagues
found that if subjects were involved in an attentionally demanding cognitive task and emotional faces (e.g., faces
that showed a fearful expression) were presented at a task-irrelevant location, amygdalar activation was significantly
reduced compared to a situation where the emotional faces were task-relevant.
Yet other results have shown that there are indeed significant automatic aspects to emotional processing. In fact,
evoked potential studies have shown that emotional response to a visual stimulus frequently precedes cognitive identi-
fication and categorization of the same stimulus. For example, Eimer and Holmes [65] found that fearful faces elicited
a positive evoked potential from the frontal and parietal cortices 121 milliseconds after stimulus presentation, whereas
face-specific visual encoding is tied to a negative potential that occurs at 170 ms.
Taylor and Fragopanagos [62] developed a network model that addressed the theoretical issues posed by these
somewhat paradoxical data. The underlying theoretical statement of their model is that emotional stimuli do not
automatically override whatever the network is paying attention to, yet emotional stimuli have a strong selective
attentional and processing advantage over nonemotional stimuli. Their model adds representations of emotionally
important brain regions to the same research group’s previous model of attentional control, a model called CODAM
(“Corollary Discharge of Attention Movement”; see [66], for a summary).
The major brain areas the Taylor–Fragopanagos model incorporates include the amygdala, as a basic processor of
emotional inputs; the ventral and orbital parts of the prefrontal cortex, which engage in higher-order processing of
emotional information (cf. [9]); and the dorsolateral part of the prefrontal cortex, which engages in complex cognitive
information processing (see Fig. 7).
In the attention/emotion network shown in Fig. 7, the amygdala can selectively boost attention paid to emotional
versus nonemotional stimuli in two different ways, both supported by known neuroanatomy and imaging results. First,
through its direct connections to the sensory areas of cortex, the amygdala can amplify the direct sensory representa-
tions of those stimuli that are emotionally significant (either positively or negatively). Second, via connections from
Fig. 7. Schematic of the attention/emotion network. OFC denotes orbitofrontal cortex; DLPFC denotes dorsolateral prefrontal cortex. (Adapted
from [67], with the permission of IEEE.)
the amygdala to both the ventral attention circuit and the orbitofrontal cortex as shown in Fig. 7, these emotional
stimuli can obtain access to the working memory representations in the dorsolateral prefrontal cortex. By the mutual
inhibition between OFC and DLPFC shown in the same figure, working memory can get “captured” by emotional
stimuli (particularly those relevant to negative emotions such as fear) and thereby get distracted from its goals.
The emotion/attention modeling of John Taylor and his colleagues is ground-breaking in the way it brings together a
large number of somewhat paradoxical results from affective and cognitive neuroscience into a few sound and intuitive
theoretical principles. It is closely connected to other work by the same group that develops biologically realistic
models of emotionally influenced cognitive tasks, such as Monchi and Taylor’s model of the Wisconsin Card Sorting
Test [68]. Yet as with every network at our current level of knowledge there are some major cognitive-emotional
processes not included in the network of [62]. For example, the inhibitory links in Fig. 7 represent opposition between
attention to stimuli that are relevant for current goals and attention to stimuli that evoke strong emotions. But if we
return to role (3) of Table 1 we see that emotions themselves are often closely tied into goals. Many human actions
are undertaken to maximize positive affect and to minimize negative affect.
Hence, strong short-term emotions often impair cognitive processing, yet long-term emotions often enhance cogni-
tive processing. A semi-quantitative network discussion of the difference between short-term and long-term emotional
responses, with reference to some results on decision making, is found in [69] (see also [70]).
The “emotional” orbital prefrontal and “task-relevant” dorsolateral prefrontal regions shown in Fig. 7 cannot
remain entirely separate for effective cognitive functioning. Rather, emotional information and task-relevance infor-
mation need to be integrated within the brain’s overall executive system, so the network can decide when to continue
fulfilling a task and when to allow urgent task-external considerations to override task fulfillment. Brain imaging
studies suggest that a third prefrontal area, the anterior cingulate cortex (ACC), plays an important role in this type
of executive integration. Posner and Peterson [71] and Posner and Raichle [72] found that the ACC is activated when
a subject must select or switch among different interpretations or aspects of a stimulus. Also Yamasaki et al. [73]
gave subjects an attentional task with emotional distractors and measured responses of different brain regions to target
(task-relevant) stimuli and to distracting stimuli. Yamasaki et al. found that while the areas with increased activation
to the two types of stimuli were largely separate, the ACC was the unique area whose activation increased to both
target and distracting stimuli.
The interactions among prefrontal executive regions (orbital, dorsolateral, and cingulate) and subcortical areas
(especially basal ganglia, thalamus, and amygdala) are also important in the recent models of emotionally influenced
decision making, which are reviewed next.
4. Models of emotionally influenced decision making
4.1. Individual decision making under risk
As Damasio’s patient studies dramatize [9], decision making is a cognitive process wherein emotional involvement
tends to be particularly significant. If humans and animals do not strictly use a common currency in comparing
alternatives, as role (4) of Table 1 suggests, at least emotion has a strong influence on the positive or negative value
(or utility) attached to alternatives.
Until the 1970s, the canonical theory of decision making assumed that decision makers calculate a utility function
that measures the desirability to them of each possible outcome. The theory further assumed that in the case of risky
alternatives (gambles), the decision maker multiplies each utility by the probability of that outcome’s occurrence, and
adds these products to get the gamble’s expected utility. The decision maker is assumed to be completely rational and
to choose the alternative whose expected utility is the largest.
Yet the results of seminal psychological experiments by Amos Tversky and the economics Nobel laureate Daniel
Kahneman (e.g., [74,75]) indicate that human decision processes violate rational utility maximizing norms in some
systematic and repeatable ways. For example, if two alternatives have equal expected utility but one of them has a
certain outcome and the other involves risk, humans tend to avoid the risky alternative if the choices both involve
gains, and to choose the risky alternative if both involve losses. Hence, if the exact same alternatives are framed in
terms of gains or losses, the choices will typically be different in the two cases even though the expected consequences
of choosing each alternative remain the same. For example, preferences among possible public health measures are
different if the choices are framed in terms of people dying versus people saved.
Some of these nonrational factors can be approached quantitatively through variations on neural network models
of animal conditioning and learning. For example, Grossberg and Gutowski [76] applied a variant of the gated dipole
(Fig. 4) to explaining some of the Tversky–Kahneman framing data. Previously, Tversky and Kahneman themselves
had developed a theory called Prospect Theory whereby preferences are a nonlinear function both of gain (or loss)
and of its probability of occurrence. But Prospect Theory excludes the context of statements and the past experience
of decision makers, whereas the network theory of [76] (called the Affective Balance Theory) considers such dynamic
variables. Recall from Section 2 that gated dipoles provide a means to compare current values of motivational or
sensory variables with expected values of those same variables. Such expectation could be based either on recent past
events or on verbally induced anticipation. The latter possibility explains Tversky and Kahneman’s data on effects of
linguistic framing on decisions.
Leven and Levine [77] extended this gated dipole model of choice to aspects of multiattribute decision making.
These authors modeled soft drink consumer preferences during the “New Coke” fiasco of the mid-1980s. New Coke
had outscored Old Coke in blind taste tests because of its sweetness, but was a failure in the market because it lacked
the familiarity of Old Coke. This suggests that the mood change due to changed context altered selective attention
among different features of soft drinks. This was modeled using a network connecting gated dipoles for features,
drives, and drink categories, with a categorization mechanism similar to that of Adaptive Resonance Theory [32],
attentionally weighted attribute vectors, and associative learning of connections between drives and attributes.
But the task most used to study emotional influences on decision making is one Antoine Bechara and his colleagues,
including Antonio Damasio, developed in the 1990s to study the decision making deficits in patients with abnormal
cognitive-emotional interconnections. This is the Iowa Gambling Task [9,78,79]. Subjects were given a sequence of
100 choices among four decks of cards that provided different gains and losses of play money. In the most common
protocol, two of these decks (decks A and B, see Table 2) had higher short-term payoffs ($100 per card as opposed
to $50 for decks C and D). However, the decks with higher short-term gains also led to long-term expected losses.
Bechara and his colleagues tested both normal subjects on this task along with patients with damage to either the
orbital prefrontal cortex (OFC) or amygdala. They found that normals begin with selections from one of the risky
decks, but gradually begin to shift towards advantageous decks as the task progresses. On the other hand, patients
with damage to either the OFC or amygdala never learn the advantageous strategy.
Several recent neural or cognitive models have reproduced some of the results on the Iowa Gambling Task (IGT)
[70,80–82]. The networks of Frank and Claus [70] and of Levine et al. [82] simulated the decision processes on this
Table 2
Decks used in the Iowa Gambling Task and their expected earnings (denoted
by “EV”)
Deck 1 (bad): $100 gain/card, p (−$1250) = 0.1 ⇒ EV/10 cards = −$250
Deck 2 (bad): $100 gain/card, p (−$250) = 0.5 ⇒ EV/10 cards = −$250
Deck 3 (good): $50 gain/card, p (−$250) = 0.1 ⇒ EV/10 cards = $250
Deck 4 (good): $50 gain/card, p (−$50) = 0.5 ⇒ EV/10 cards = $250
task by means of a network composed of analogs of several parts of the prefrontal cortex and associated subcortical
regions. In [82], the network’s dynamics are described by shunting nonlinear equations similar to those used in the
conditioning models discussed in Section 2.
The brain regions involved in modeling the IGT start with the amygdala, as the main locus for encoding emotional
positive and negative valences of stimuli or potential actions. The orbital prefrontal cortex, the region damaged in
Damasio’s patients [9], plays the role of updating these emotional valuations as learning takes place [83]. The basal
ganglia, particularly the area of ventral striatum called the nucleus accumbens (NAcc), are required for converting
emotional valuations into influences on action. Two pathways project from basal ganglia to thalamus, which in turn
projects to the cortex thence back to the basal ganglia; these are the direct pathway (two levels of inhibition) which
activates motor behavior, and the indirect pathway (three levels of inhibition) which inhibits motor behavior [84].
Finally, learning or updating reward values of stimuli requires the neurotransmitter dopamine. Dopamine cells initially
respond to primary reward, but gradually shift their responses to a conditioned reinforcer [85], which in this case is
a card deck that the subject learns is rewarding. Recall from Section 2 that the dopamine neurons are involved in
responses to unexpected rewards [58,59].
Hence, risky decisions involving gains and losses tend to be based not only on how much a person anticipates
winning or losing, but how much those expected gains and losses are higher or lower either than previous expectations,
from the consequences of a different outcome of the same gamble, or than the consequences of a choice of a different
gamble. Such calculations of gains and losses relative to context are known to decision psychologists as counterfactual
comparisons [86].
In fact, brain imaging studies have begun to verify human encoding of counterfactual comparisons. Breiter and his
colleagues [87] presented human subject with either a “good” lottery (equal chances of winning $10, $2.50, or $0);
an “intermediate” lottery (equal chances of winning $2.50, winning $0, or losing $1.50); or a “bad” lottery (equal
chances of winning $0, losing $1.50, or losing $6). Breiter et al. found that a particular subcortical emotion-sensitive
region (a part of what is called the extended amygdala) responded differently to a $0 outcome depending on which
lottery (good, intermediate, or bad) the subject had been shown.
As more studies are done, it seems likely that counterfactual comparisons will activate the usual neural interactions
involving dopamine neurons and the basal ganglia as well as primary emotional areas. For this reason, both the gated
dipole network (Fig. 4) and the temporal difference network (Fig. 3) have proved fruitful in modeling contextual
aspects of emotional influences on decision making.
More recently, many researchers have come to the conclusions that animals foraging for food also use these kinds of
emotionally influenced calculations to make decisions about where to search. For example, an animal must sometimes
decide between one patch that contains a highly desirable food but entails a significant predation risk, and another
patch that contains a less desirable but still nourishing food and is relatively safe from predators. This has generated
some neural network models of foraging behavior based both on temporal differences [88,89] and on gated dipoles
[90].
Foraging theory, like the theory of human decision making, has been heavily influenced by optimality considera-
tions. As reviewed in [88–90], optimal foraging theories have been based on the assumption that an animal’s foraging
decisions are the ones that maximize its lifetime survival probability. Yet there is considerable evidence that foraging
decisions may deviate from lifetime fitness maximization due to consideration of short-term risks, both of starvation
and predation [91–93].
Niv et al. [88,89] replicated a pattern of risk aversion in foraging bees using a neural network reinforcement learning
paradigm based on temporal difference ideas, combined with genetic algorithms, obviating the need for a nonlinear
utility function such as found in some nonneural decision models. Coleman et al. [90], using a variant of the gated
dipole (see Fig. 8), simulated short-term emotional reactions that could at times include risk aversion for gains and
risk seeking for losses. The survival rate of the “cognitive-emotional forager” of [90] was less than that of optimal
foraging models but surprisingly close to the optimal rate.
4.2. Social influences and long-term behavioral development
Thus far, neural network models of decision making have largely neglected the personality characteristics of the
decision maker. Ultimately, individual differences will need to be included for a full account of the phenomena of
emotionally influenced decision making. For example, Peters and Slovic developed a modified form of the Iowa
Fig. 8. Two gated dipoles, as in Fig. 4, are combined to create a multiattribute cognitive-emotional forager model in which the outputs of pairs
of opposite affective components are summed. Unlike the dipole in Fig. 4, each dipole can receive either an emotionally positive input J + and
an emotionally negative input J −. The two channels in one dipole, labeled Food-finding dipole, represent finding and not finding food. The two
channels in the other dipole, labeled Predator avoidance dipole, represent avoiding and being subject to predation. Behavioral output is based on
positive emotional signals from both dipoles. (Adapted from [90] with the permission of the Psychonomic Society.)
Gambling Task designed to dissociate the variables of maximum gain, maximum loss, and expected value [94]. Peters
and Slovic found that subjects with extroverted personality profiles tended to prefer high maximum gain alternatives,
whereas subjects with cautious personality profiles tended to avoid high maximum loss alternatives. The large number
of parameters in the types of neural networks discussed here allows such networks ultimately to simulate variable
choice profiles based on these types of personality differences.
In fact, there have been preliminary, not yet quantitatively simulated, neural network theories of large-scale
behavioral patterns, including contextual activation of cooperative versus competitive patterns [95] and character
development in the course of an individual’s life [96–98]. My current articles [96,97] develop a theory of how peo-
ple and animals make decisions about what actions to perform and what actions to refrain from performing, based
on a complex interaction between emotional signals and task-oriented signals. Most of the fragments of that theory
are based on facts that are generally accepted now among cognitive neuroscientists, and the connections between
fragments are suggested by previous neural network models of more circumscribed processes.
The theory of decision among large behavioral patterns, elaborated in [96,97], is sketched here in general terms.
First, developmental experiences, such as a pattern of exposure to caring or abuse as a child, predispose people as
adults to be biased toward one or another of these behaviors. Since the orbital prefrontal cortex (OFC) is the main
cortical processing area for social and emotional information [9], pathways connecting OFC and various subcortical
regions are a likely substrate for developmental (and cultural) influences on prevailing behavior patterns. The notorious
19th century patient Phineas Gage lost the ability to make plans and appropriate social responses after being injured
in the OFC by a railroad accident. From Gage’s case and other patient studies [9], as well as animal lesion studies,
neuroscientists believe OFC forms and sustains mental linkages between specific sensory events in the environment
(e.g., people or social structures)—and positive or negative affective states. This region creates such linkages via
connections between neural activity patterns in the sensory cortex that reflect past sensory events, and other neural
activity patterns in subcortical regions (e.g., amygdala and hypothalamus) that reflect emotional states.
How are these positive and negative emotional linkages translated into behavior patterns, that is, into action ten-
dencies or avoidances? This is done via the gating system in pathways between the prefrontal cortex, basal ganglia,
Fig. 9. Left side: Loops between nucleus accumbens, thalamus, and cortex for gating behaviors. Nucleus accumbens selectively disinhibits action
representations by inhibition of the ventral pallidum, thereby releasing signals from thalamus to cortex. Right side: influences on the selective gating
from hippocampus (context), amygdala (emotion), and prefrontal cortex (planning). (Adapted from [99] with permission from Elsevier Science.)
and thalamus [84,99] (Fig. 9). The link from basal ganglia to thalamus allows contextual signals to selectively release
from inhibition the neural signals for performance of actions whose representations are usually suppressed.
How might individual differences in personality influence these choices? The research psychiatrist Robert
Cloninger [100] described the components of character (largely learned during development) as follows: self-
directedness (acceptance of the self); cooperativeness (acceptance of other people); and self-transcendence (accep-
tance of nature). Cloninger described eight possible personality profiles as characterized by high or low values of these
three character parameters, with the healthiest state (which he called creative) exhibiting high values of all three of the
character components. These personality profiles were interpreted in [96] as attractors for a high-dimensional system
representing connection strengths at many brain loci (a system that includes the three prefrontal executive areas of
OFC, dorsolateral prefrontal, and anterior cingulate).
The goal of psychotherapy or other interventions in a person’s life can be described in neural network terms
as moving the individual from other attractors toward the creative attractor. Switches from less to more optimal
states have been described in neural networks by simulated annealing [101], which is based on a noise signal that is
strongest when the system is furthest from an optimal state. My network theory of self-actualization [102] is based
on a continuous stochastic dynamical system version of simulated annealing; mathematical studies of this process, by
Leon Hardy and me, are in progress. This is often described as moving from a local to a global minimum of a system
function, known mathematically as a Lyapunov function.
One of the simpler general neural systems possessing a Lyapunov function is the Cohen–Grossberg system [103]
based on self-excitation and mutual inhibition, described by the equations

dxi
n
= ai (xi ) bi (xi ) − cik dk (xk ) , i = 1, . . . , n (3)
dt
k=1
which are a generalization of the lateral inhibition equations (2). As time increases, the system (3) always converges
to a steady state (point attractor) because the Lyapunov function, called V , decreases along trajectories. The Lyapunov
function for (3) is
n

xi
1
n
V (x) = − bi (ξi )di (ξi ) dξi + cj k dj (xj )dk (xk ). (4)
2
i=1 0 j,k=1
Fig. 10. An individual’s needs form a competitive module. If the current state of the module has a larger V function than some alternative state
detected by the world modeler, the net signal (excitatory minus inhibitory) to the creative discontent node is positive. The discontent node sends
noise which perturbs the needs module so it can move toward a different attractor. (Adapted from [102] with the permission of Lawrence Erlbaum
Associates.)
Hence, the steady state approached is either a local minimum or the global minimum for the function V defined by (4).
The global minimum can be interpreted as an optimal state, and local minima as less optimal states.
Levine [102] interpreted a competitive network such as the one defined by (3) as encoding fundamental needs
of the organism, which compete via lateral inhibition as in Fig. 10. The Lyapunov function V is interpreted as an
overall “distress level” from unmet needs of the network or organism. This competitive module is supervised by a
“world modeler” module, possibly analogous to working memory areas in the dorsolateral prefrontal cortex. The
world modeler imagines and makes “copies” of various possible states of the need subsystem and calculates the
Lyapunov function for each, in search of a state with a lower V . If V of the current state, say x, is larger than V
of some other projected state, say x0 , the combination of excitation from the needs module and inhibition from the
world modeler produces a signal of magnitude V (x) − V (x0 ) to a “creative discontent” module. When thus activated,
the discontent module in turn sends random noise back to the needs module, which can move that module out of a
suboptimal local minimum. The strength of this discontent signal, and thereby the amount of tendency to move toward
an optimum, is partly regulated by the level of the neurotransmitter norepinephrine, which has been associated with
personal initiative and combating learned helplessness [104].
But this “needs module” is just a part of a much larger network including representations of action patterns, because
each state of the needs system has to interact with contexts to generate performance or nonperformance of behaviors.
Behaviors that we decide to perform go through, and behaviors that we decide to avoid are actively barred from,
gates at the nucleus accumbens (Fig. 9). The hippocampus activates representation of current context, which in turn
activates behavioral approach and avoidance representations relevant to that context. Longer-term storage of affective
valences is likely to be at connections from orbitofrontal cortex to amygdala [82]. Changes that affect behavior (“do”
and “don’t” instructions, approach toward or avoidance of an object) are likely to be at connections from amygdala to
medial prefrontal cortex (incentive motivation) and from orbitofrontal to nucleus accumbens (habit).
The preceding sections have summarized models of the influences of positive and negative emotional valences on
common psychological processes (conditioning, attention, and decision making). The next section will describe a few
models of particular types of emotion.
5. Models of specific emotions
Most of the research done so far on neural network modeling of emotion has differentiated positive versus negative
affect, but otherwise has been relatively nonspecific. Neural network modeling of specific emotions (fear, sadness,
joy, disgust, anger, surprise, etc.) is just starting to emerge.
Fig. 11. Basic model of fear conditioning. Nodes within each area compete by lateral inhibition. The nodes with highest activity in each brain
region are denoted by black squares, the less active nodes by white squares. “Lemniscal” and “extra-lemniscal” refer to different parts of the
auditory thalamus. (Adapted from [107] with the permission of the American Psychological Association.)
5.1. Models of fear conditioning
Of all the basic emotions, the one that has so been most studied neurobiologically is fear. This is mainly due to
the pioneering studies of fear responses and fear conditioning by the neuroscientist Joseph LeDoux [105,106]. The
results from LeDoux’s laboratory inspired a series of brain-based neural network models of auditory fear conditioning
by Jorge Armony and his colleagues [107–110].
Armony’s basic modeling structure is schematized in Fig. 11. The model includes both cortical and subcortical
influences on the amygdala, both of whose weights are modified by conditioning (that is, by pairing of an auditory
CS with a noxious US). As reviewed in [105], there are parallel cortical and subcortical pathways that reach the
primary emotional processing areas of the amygdala. The subcortical pathway is faster than the cortical, but the
cortex performs finer stimulus discrimination than does the thalamus. This suggests that the two pathways perform
complementary functions: the subcortical pathway being the primary herald of the presence of potentially dangerous
stimuli, and the cortical pathway performing more detailed evaluations of those stimuli.
Armony et al. [107,108] reproduced a great many detailed experimental results on the responses of single neurons
in different brain regions during fear conditioning experiments. In [109] they noted one surprising prediction of the
model that later was experimentally verified. Because of the poor discriminative ability of neurons in the auditory
thalamus compared with neurons in the auditory cortex, it had been expected that auditory cortex lesions would cause
the learned fear responses to generalize more broadly to auditory stimuli other than the original CS. Yet when the
auditory cortex of the model network was “lesioned”, the generalization properties of the network were unaffected.
This surprising lack of an effect on generalization was later confirmed by behavioral studies in lesioned rats. Their
explanation of the surprising finding was that even if individual thalamic neurons were poor discriminators, the total
population of thalamic neurons could discriminate among stimuli with sufficient accuracy to compensate for the loss
of the cortex.
5.2. A model of positive affect
Thus far, none of the other emotions has been studied biologically in as much detail as LeDoux and his colleagues
have studied fear. In particular, there have not been comparable studies of positive emotions such as joy. However,
Ashby et al. [111] developed a neurobiological theory to explain the experimental psychologist Alice Isen’s results
showing that induced positive affect enhances creative problem solving and cooperative behavior (see [112] for a
review). Ashby and Isen [113] simulated aspects of this theory in an unpublished computational model. It is to be
noted that the positive affect that Isen found to improve cognitive flexibility, and thereby improve creativity, was not
the intense pleasure that follows falling madly in love or winning the lottery. It was the relatively mild positive mood
that can be experimentally induced by a variety of means, such as receiving an unexpected piece of candy, finding a
coin in a pay telephone, or watching a humorous video.
The evidence reviewed in [111] points to various ways that mild positive affect promotes creativity. On cognitive
tasks, positive affect leads to more exploration of alternatives and thereby promotes the ability to see unconventional
ways of solving a problem. An example of this kind of unconventional thinking is a task wherein the subject is asked
to attach a candle to a wall given matches and a box of tacks. The solution to this task requires using both the tacks
and the box itself [114]. Also, positive affect leads to expansion of possible membership in a category, particularly a
favorable category; for example, people that one normally perceives as being members of an “out group” may instead
be perceived as part of one’s “in group”.
As in the animal reward learning models discussed earlier [59,60], in the model of [113] the key neural transmitter
for positive affect, and for its salutary cognitive effects, is dopamine. (Since then, evidence has been found that the
connection of dopamine with positive affect does not have to do directly with actual feelings of pleasure but with
incentive motivation toward rewarding stimuli [115]; because the Ashby–Isen model deals with cognitive effects
rather than with direct emotional experience, that is probably not an argument against their theory.) Ashby et al.
noted that positive affect is different from nonspecific arousal. Arousal is linked not to dopamine but to a different
neurotransmitter, norepinephrine. Also, at the psychological level, Isen and her colleagues found that creative problem
solving is facilitated by positive affect but not by other arousing processes such as negative affect (induced by a film
about the Holocaust) or physical exercise [116]. Finally, arousal tends to increase the probability of an individual’s
dominant responses, rather than unconventional or creative responses.
The neural theory Ashby et al. [111] developed for the creative effects of positive affect is based on increased
dopamine signals to two brain executive regions discussed in previous sections: the dorsolateral prefrontal cortex
(DLPFC) and anterior cingulate cortex (ACC). Their detailed neural network also involved parts of the basal ganglia
that receive dopamine signals and are involved in attentional and behavioral choices, and some biochemical processes
at the neuronal level involving membrane receptors and second messengers.
Another source of information about the details of emotional and affective processes is from studies of mental
conditions in which these emotional processes are impaired. The literature on modeling of mental illnesses has grown
rapidly in the last decade, and the next section provides only the “flavor” of that work and not an exhaustive summary.
6. Models of emotional disorders
Artificial neural networks have sometimes been used or proposed as diagnostic tools for mental and emotional
disorders as well as for other types of diseases. This involves training a network (usually of the back propagation
variety) to recognize a particular disease from classes of symptom vectors characteristic of known cases of the disease.
However, we do not discuss that type of network here. Rather, as in other sections of the article we confine our
attention to models that implement theories of the underlying mechanisms associated with the disease or with its
behavioral manifestations. In the more recent models, this typically includes brain regions and processes that the
disease characteristically impairs. This type of brain-based theory has been suggested as a novel form of disease
assessment [117,118].
The classification of mental and emotional disorders agreed on by psychiatrists is far from scientifically precise.
Hence, the familiar classifications are subject to change as more knowledge comes from neuroscience in the years
ahead. The dialogue between clinical psychiatry and basic neuroscience has become much more extensive in the last
decade due to the rapid development of brain imaging technology. This dialogue has included several conferences and
collections of articles about neural network modeling of mental disorders (e.g., [118–122]).
Every computational theory of a network structure designed to perform specific psychological functions is depen-
dent on the network parameters lying within some range that enables those functions to be performed properly; in
some cases, that range can be explicitly characterized mathematically. Consequently, the same network with parame-
ters outside that range exhibits characteristic pathologies of the functions the network is designed to perform. As the
theory becomes more refined, and more closely tied to neuroscience, the mapping of such pathologies will continue to
be a growth industry for several decades. Yet some examples already appear in the literature and have drawn interest
from the clinical community.
6.1. Overarousal and underarousal, schizophrenia, and autism
Grossberg in several articles found that pathologies of the gated dipole (Fig. 4; Eq. (A.2) of Appendix A) are
analogous to various mental and neurological disorders. He showed mathematically that in the gated dipole, if the
nonspecific arousal (input I of Fig. 4) is within a certain range, the network mimics what is usually considered normal
behavior [123]. When I is below the minimum of that range, its threshold of response to limited-duration inputs
is raised. Paradoxically, once this threshold is exceeded, the on channel activity (see Fig. 5) of the gated dipole is
hypersensitive to input increments. Giving the network a “drug” that increases nonspecific arousal (analogous to an
“upper”) reduces these “symptoms” of hypersensitivity. But if too much of the upper is administered, the network can
develop the opposite syndrome associated with overarousal. Grossberg compared underarousal effects in his network
to observed symptoms of both juvenile hyperactivity and Parkinsonism. These illnesses are frequently treated by
drugs that enhance the efficacy of the neural transmitter dopamine—Ritalin (or, in 1984 when the article was written,
amphetamine) for hyperactive children, and L-DOPA for Parkinson patients. The side effects of overly large doses
of those drugs can include schizophrenic-like symptoms. Conversely, some drugs used to treat schizophrenics by
suppressing dopamine have Parkinson-like side effects.
The effects of overarousal in this network are opposites of some underarousal effects. The threshold for response
to a limited-duration input is reduced. But once the threshold is achieved, the network is abnormally insensitive to
increments in input intensity. This is analogous to the flatness of affect characteristic of some kinds of schizophrenia,
as developed further in a recent article [124].
Grossberg and Seidman [37] proposed a network theory of autism (putting together a spectrum of autistic-family
disorders) that includes gated dipole underarousal among other network “symptoms”. The underarousal leads, as
stated before, to hyperexcitability: the tendency of autistic individuals to react with overly strong negative emotion to
some kinds of motivationally irrelevant differences from established patterns.
But the full spectrum of autistic symptoms, including deficits in language and in social interaction, also depends
in Grossberg and Seidman’s theory on two other network abnormalities. One of them involves the categorization
mechanism derived from Adaptive Resonance Theory [65], which includes a parameter called vigilance that measures
how close an input must be to a category prototype to be accepted as a member of the category. Many autistics
exhibit a kind of “hypervigilance”, in that their criteria for category membership are overly stringent because this
vigilance parameter is pathologically high, so the irrelevant differences among objects or events are given excessive
importance. Another abnormality involves a timing mechanism, which Grossberg and Schmajuk first developed in
their classical conditioning model [42]. Later articles (e.g., [125]) located the response part of the timing mechanism
in the cerebellum, which has been found to be abnormal in many autistics, and this timing deficit could be one reason
for these individuals’ difficulty in reading and communicating social cues.
The Grossberg–Seidman theory of autism is a significant advance that still leaves many open problems. The authors
note that they are simply describing a set of network pathologies but not suggesting an underlying (genetic or envi-
ronmental) cause for the disease. Finding such a probable cause would be likely to illuminate the biological process
whereby a diverse collection of symptoms (emotional hyperexcitability above threshold, cognitive hypervigilance,
and impaired adaptive timing) become associated in the same individual.
6.2. Excitatory-inhibitory imbalance, manic-depression, and unipolar depression
Network pathologies also form the basis for a theory of manic-depressive illness by David Hestenes [126]. Hestenes
described this disorder and a few others as malfunctions of the balance between excitation and inhibition in a network
similar to the Adaptive Resonance Theory (ART) network [32]. ART involves an interaction of two levels of nodes;
typically, one level (“bottom”) represents primary sensory processes and is based on shunting lateral inhibition with
equations that are a variant of (2), and the other level (“top”) regulates interactions at the bottom level by means of
executive attentional control. Hestenes adduced evidence that aspects of top-down regulation in an ART model are
analogous to modulation by the neurotransmitters dopamine (DA) and serotonin (5-HT). A 5-HT deficit can lead to a
sensory network with too little inhibition, producing hallucinations or mania. A DA deficit can lead to a lower-level
network with too little excitation, producing anhedonic depression. In his theory a particularly important locus for
these transmitter malfunctions is the nucleus accumbens, the part of the basal ganglia which has closest connections
with the emotionally related regions of amygdala and orbital prefrontal cortex, and thereby functions as a gate for
activating or suppressing behaviors based on their likely emotional consequences (see Fig. 9).
Hestenes’ article [126] does not include quantitative simulations, yet remains one of the most comprehensive and
theoretically sound treatments of the network basis for an emotional disorder. Hestenes also includes a description of
the effects on an actual patient of a treatment regimen that his theory suggested: a judiciously timed alternation of
tryptophan (the amino acid which is a biochemical precursor of 5HT) for treatment of manic symptoms, and tyrosine
(the amino acid precursor of DA) for treatment of depressive symptoms. He extended his network theory in a later
article to account for some of the cognitive malfunctions involved in mania [127].
A series of network models of depression by Greg Siegle and his colleagues (see [128] for a detailed description,
and [117] for review of the models’ functional significance), illuminate the interrelationships between cognitive and
affective aspects of depression. These models deal with unipolar depression, that is, clinical depression that does not
alternate with mania.
The quantitative simulations of Siegle’s models include nodes that are not explicitly considered as brain regions
but whose functional architecture incorporates three basic processes that are analogous to brain mechanisms involved
in depressive symptoms. The first process is overlearning, that is excessive associative weight, of learned connec-
tions between representations of particular stimuli or events and representations of negative emotions. The second
process is reduced strength of inhibitory connections from executive areas of the left dorsolateral prefrontal cortex
to representations of negative emotions in the amygdala. (There is considerable evidence from recent brain imaging
and clinical studies of a laterality distinction in brain representations of emotions, with the left hemisphere of the
brain relating more to positive affect and the right hemisphere to negative affect.) The third process is rumination:
continuing to dwell on negative and pessimistic thoughts, which was implemented by reverberating positive feedback
loops between emotional and cognitive representations.
It is not certain how close we are to the goal of having neural network models that are a useful tool to aid psy-
chiatrists and clinical psychologists in their diagnoses. Yet modeling is an increasing part of the ongoing process of
deepening our biological understanding of the brain processes and transmitters involved in mental and emotional dis-
orders. The caveat must be added, though, that insights derived from neural networks should not be used as argument
for a complete “medicalization” of psychiatric treatment, in other words, for supplanting verbal therapy by drug ther-
apy. Rather as we understand brain processes better through network approaches, we are likely to get a better handle
on the precise ways in which both verbal and drug treatment influence the dynamics of those processes. This has led
to a few network-inspired ideas about how the practice of verbal psychotherapy might be made more effective and
supportive [97,129].
7. Concluding remarks
For a long time emotion was a difficult area for quantitative cognitive modeling, in part because it was mysterious
and hard to define precisely (for a partial history see [130]). Yet both neuroscientists and neural modelers gradually
learned to distinguish between the neural mechanisms of emotion and the nature of emotional feelings [105,109], and
found that the former was suitable for modeling. Just as it is not necessary to fully understand the experience of seeing
a color to map the neural dynamics of color vision, it is not necessary to fully understand the conscious experience of
joy, sadness, fear, or anger to map the neural dynamics of those emotions (even more, the neural dynamics of positive
and negative affect in general).
As emotions have been related to characteristic action patterns, and to neural processes characteristic of specific
brain regions and circuits, emotions have become as amenable to neural network modeling as any other psychological
processes [26,131]. Neural networks have particularly made significant contributions to understanding the complex
interactions of emotion with cognitive processes such as attention, decision making, and memory.
The results of neural network investigations support philosophical outlooks that regard cognitive processes as
inextricable from emotion [19,132–134]. The cultural conventional wisdom that emotion and reason are opposites
has been decisively refuted. Yet overly strong emotions, positive as well as negative, can interfere with effective task-
oriented behaviors in the short run; the behavioral gates at the nucleus accumbens gates receive strong signals that
represent task-relevance (from the hippocampus) as well as strong signals that represent emotional salience (Fig. 9),
and the two types of signals may compete [97,99]. But the long-term effects of emotions are often more positive
[69]. It is difficult to achieve professional goals without enjoyment of one’s work, or personal goals without love for
significant others.
Of course, in a review article such as this one, it is necessary to omit a significant amount of important research
related to the article’s theme. Not only does space not permit coverage of all major emotional phenomena, but the
selection must be biased toward those phenomena for which computational models have already been developed, or
at least proposed in detail.
In particular, I have only sketched a little of the work that bears on the social and interpersonal aspects of emotion.
The expressive and communicative aspects of emotion, which are important for the formation of social bonds [15,
132], are not discussed here. Nor are the aesthetic emotions that attend the need for knowledge and for making sense
of the world, emotions that can generate cognitive dissonance when that need for knowledge is thwarted and artistic
or intellectual pleasure when the need is met [133]. Also, my coverage of neural network models of mental disorders
focuses mainly on the emotional aspects of those disorders and says little about the cognitive aspects; in particular,
about deficits in performance on specific cognitive tasks used by clinicians. Other readers will no doubt disagree with
some of the other omissions in this article.
Yet my goal has been to communicate the gist of an ongoing enterprise, rather than to be complete or comprehensive
about a part of that enterprise. The study of emotion is inherently interdisciplinary, involving insights from psychology,
philosophy, social sciences, neuroscience, and now neural networks. In order to understand this complex and intricate
set of phenomena we must search for what the evolutionary biologist Edward O. Wilson [135] calls consilience: a set
of principles and system understandings that is self-consistent across different disciplines and the different levels of
understanding those disciplines foster (see also [24,136]). Since the common language of mathematics often enhances
the possibility of this kind of interdisciplinary consistency, we can expect future, more accurate neural network models
of emotion to play a major part in creating the emerging consilience.
Acknowledgement
I am pleased to acknowledge several colleagues who have made contributions of significant positive emotional
valence to the work in this review, as collaborators in research or fellow participants in workshops or both. These
include A. Aleksandrowicz, Y. Choe, R. Eisler, S. Estrada, S. Grossberg, N. Jani, R. Kozma, S. Leven, D. Loye,
B. Mills, L. Perlovsky, V. Reyna, J. Taylor, and P. Werbos.
Appendix A
The equations for the network of Grossberg and Levine [29], involving classical conditioning combined with lateral
inhibition, based on the diagram in Fig. 2. The interacting variables are the first stage of stimulus representations (for
CS1 , CS2 and US), xi1 , i = 1, 2, 3; the second stage of stimulus representations, xi2 , i = 1, 2, 3; the drive representa-
tion y; and the weights between stimulus and drive representations, wig , i = 1, 2, 3. For simplicity the weights from
xi1 to y (representing conditioned reinforcement) and the weights from y to xi2 (representing incentive motivation)
were telescoped into one set of weights, since in the network the two sets of weights tend to vary together.
The representations at the first stage, xi1 , undergo shunting recurrent interactions similar to those of Eq. (2) for
general lateral inhibitory networks. That is
dxi1
= −Axi1 + (B − xi1 )Ii1 − xi1 Ji1 (A.1a)
dt
where Ii1 denotes total excitatory input to xi1 and Ji1 . The total excitatory input is a sum of an external CS or US
signal; a positive feedback signal from xi1 to itself; and a positive feedback signal from xi5 to xi1 . The feedback signal
functions are ramp functions, the simplest type of sigmoid functions (see Fig. 12). A ramp function is defined in terms
of parameters α (the threshold) and β (the saturation point) by
0, x α,
R(x; α, β) = x − α, α < x β, (A.1b)
β − α, β < x.
Fig. 12. Ramp function with threshold α and saturation point β.
The positive feedback signal from xi1 to itself triggers a process of habituation that is modeled for simplicity as an
exponentially decaying function of time, rather than a habituating transmitter gate as in the gated dipole of [26]. This
exponentially decaying function of time is multiplied by the sum of the two ramp function signals, leading to a total
excitatory input of

Ii1 = Ii + C R(xi1 , α1 , β1 ) + R(xi2 , α2 , β2 ) exp −D(t − Ti − E)+ (A.1c)
where C, D, E, αi , and βi are positive constants; Ii is the ith stimulus input; Ti is the onset time of Ii after each input
presentation; and the function [w]+ denotes max(w, 0).
The total inhibitory input Ji1 is the sum of ramp signals from the other node activities, namely

Ji1 = F R(xj 1 ; α1 , β1 ) (A.1d)
j =i
with F another positive constant. Combining Eqs. (A.1a) through (A.1d) yields the total equation for the first stage
stimulus nodes:
dxi1

= −Axi1 + (B − xi1 ) Ii + C R(xi1 , α1 , β1 ) + R(xi2 , α2 , β2 )
dt

+
× exp −D t − Ti − E − F xi1 R(xj 1 , α1 , β1 ) (A.1e)
j =i
for i = 1, 2, 3.
The drive representation, y, is similarly activated by a ramp function of the total of inputs from the stimulus
representations multiplied by their weights:
3
dy
= −Hy + KR GR(xj 1 ; α1 , β1 )wj , α3 , β3 . (A.1f)
dt
j =1
The second set of stimulus representations, xi2 , are activated by the combination of ramped signals from the
corresponding xi1 and from y, gated by the weight between them, as follows:
dxi2
= −Lxi2 + MR(xi1 ; α4 , β4 )R(y; α5 , β5 )wi (A.1g)
dt
for i = 1, 2, 3.
Finally, the weights from the CS stimuli to the drive obey a similar law to (A.1g), except with a much slower decay
rate (in the case of our simulations, L = 3 and N = 0.05):
dwi
= −Nwi + P R(xi1 ; α1 , β1 )R(y; α6 , β6 ). (A.1h)
dt
The equations for the gated dipole of Fig. 4 (see [26]), with the nodes as listed in the figure, are
dy1 dy2
= −ay1 + I + J, = −ay2 + I,
dt dt
dw1 dw2
= b(c − w1 ) − ey1 w1 , = b(c − w2 ) − ey2 w2,
dt dt
dx1 dx2
= −f x1 + gy1 w1 , = −f x2 + gy2 w2 ,
dt dt
dx3 dx4
= −hx3 + k(x1 − x2 ), = −hx4 + k(x2 − x1 ),
dt dt
dx5
= −mx5 + k(x4 − x3 ). (A.2)
dt
Eqs. (A.2) were written under the assumption that the “negative” channel is the one receiving the emotionally sig-
nificant input J , as in the case of relief from electric shock. If instead the “positive” channel receives the significant
input, then the term I + J in the equation for y1 is replaced by I , and the term I in the equation for y2 is replaced
by I + J . In a variant of the gated dipole the signals received by x3 , x4 , and x5 are constrained to be positive or zero;
hence each of the terms x1 − x2 , x2 − x1 , and x4 − x3 is replaced by 0 if it becomes negative.
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Physics of Life Reviews 4 (2007) 37–63

Neural network modeling of emotion

Keywords: Neural networks; Emotion; Cognition; Behavior; Dynamical systems

1. Introduction: the uses of emotion and affect . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38

* Tel.: +1 817 272 3598; fax: +1 817 272 2364.

4.1. Individual decision making under risk . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48

1. Introduction: the uses of emotion and affect

2. Early models of Pavlovian conditioning

2.1. Theoretical foundations of neural networks

2.2. Associative learning models in conditioning

ȳ(t) (representing a weighted average of past output activities):

x̄i (t + 1) = α x̄i (t) + xi (t),

3. Models of emotional influences on attention

4. Models of emotionally influenced decision making

4.1. Individual decision making under risk

4.2. Social influences and long-term behavioral development

5. Models of specific emotions

5.1. Models of fear conditioning

5.2. A model of positive affect

6. Models of emotional disorders

6.1. Overarousal and underarousal, schizophrenia, and autism

6.2. Excitatory-inhibitory imbalance, manic-depression, and unipolar depression

Fig. 12. Ramp function with threshold α and saturation point β.

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