LEARNING AND MEMOMY IN BIOLOGICAL PERSPECTIVE

Reflexes

 involuntary responses to stimuli.

 behaviors are produced by prewired neural connections or reflex arcs.
 have the advantage of producing rapid, reliable responses, but their inflexibility can be a
disadvantage when the environment changes.
Instincts

 A stereotyped pattern of behavior elicited by particular environmental stimuli.

 Like reflexes, instincts are automatic
 behaviors involve mating or parenting behavior
 Although somewhat modifiable by experience, instinctive behaviors are
 consistent enough to be referred to as fixed action patterns.
Learning

 A relatively permanent change in behavior or the capacity for behavior due to experience.
 relatively permanent change in behavior (or the capacity for behavior) due to experience,
provides organisms with the most flexible means for responding to the environment.
 The requirement that learning be “relatively permanent” excludes brief or unstable changes in
behavior.
 Our definition of learning specifies that only those behavioral changes that result from experience
will be considered learned.

TYPES OF LEARNING - Learning occurs in one of two ways.

Associative learning

 occurs when an organism forms a connection between two features of its environment.
 A type of learning that involves the formation of a connection between two elements or events.
 Classical conditioning, which allows organisms to learn about signals that predict important
events,
Nonassociative learning

 A type of learning that involves a change in the magnitude of responses to stimuli rather than the
formation of connections between elements or events.
 including the processes of habituation and sensitization, involves changes in the magnitude of
responses to stimuli rather than the formation of connections between specific elements or events.
Habituation

 A type of learning in which the response to a repeated, harmless stimulus becomes progressively
weaker.
 occurs when an organism reduces its response to unchanging, harmless stimuli.
Sensitization

 A type of learning in which the experience of one stimulus heightens response to subsequent
stimuli.
 occurs when repeated exposure to a strong stimulus increases response to other environmental
stimuli.
Classical conditioning

 A type of associative learning in which a neutral stimulus acquires the ability to signal the
occurrence of a second biologically significant event.
 organisms learn that stimuli act as signals that predict the occurrence of other important events.
 The term conditioned refers to the presence of learning, whereas unconditioned refers to factors
that are innate or unlearned.
Conditioned stimulus (CS)

 In classical conditioning, an initially neutral event that takes on the ability to signal other
biologically significant events.
 refers to an environmental event whose significance is learned
Unconditioned stimulus (UCS)\

 In classical conditioning, an event that elicits a response without prior experience.

 has innate meaning to the organism.
Conditioned responses (CR)

 In classical conditioning, a learned reaction to the conditioned stimulus.

 are those behaviors that must be learned
Unconditioned response (UCR)

 In classical conditioning, a spontaneous unlearned reaction to a stimulus without prior

experience.
 appear without prior experience with a stimulus.

Reflexes, instinctive behaviors, and learning fall along a continuum of flexibility. Reflexes produce
rigid pattern of response, whereas the flexibility of learned behaviors is well suited to rapidly changing
environments. Major types of learning include habituation, sensitization, and conditioning. Classical
Conditioning of Fear. Participation of the amygdala in classically conditioned fear response in rats.
Participation of circuits in the cerebellum, including the interpositus nucleus, in the conditioning of
skeletal reflexes such as the eyeblink. Participation of forebrain structures in trace conditioning.
Memory

 commonly refers to the storage and retrieval of information

Information processing models - The Atkinson-Shiffrin Model of Memory

 theories of memory that seek to explain the management of information by the brain, from
detection to storage to retrieval.
 memory assume that information flows through a series of stages on its way to permanent storage
in memory,

The Atkinson-Shiffrin Model of Memory

Sensory memory

 An initial stage in memory formation in which large amounts of data can be held for very short
periods.
 any information sensed by an organism initially enters the sensory memory.
 This first memory stage can hold a large amount of data for a very brief period of time, on the
order of a few seconds.
 From this initial set of data, we select information for further processing and move it to the next
stage of memory, the short-term memory.
Short-term memory or “working” memory.

 An intermediate memory store in which limited amounts of data can be held for a limited amount
of time; without further processing, such information is permanently lost.
 This stage contains all the data that we are currently thinking about.
 Has a very limited capacity, somewhere between five and nine unrelated items. When we try to
add additional items, previous information is often lost.
 lost rapidly, in 15 to 18 seconds
 it is sorted into temporary storage areas or buffers for auditory, visual, or combined types of
information, which are managed by a “central executive” process
Long-term memory

 A memory store in which apparently unlimited amounts of data can be held for an unlimited
amount of time.
 seems to have few, if any, limitations on capacity or duration.
LONG-TERM MEMORIES ARE DIVIDED INTO THREE CATEGORIES:
Semantic memory

 A type of declarative, explicit memory for facts and verbal information.

 contains basic knowledge of facts and language.
Episodic memory

 A type of declarative, explicit memory for personal experience.

 remember the episodes of your life
Procedural memory

 A type of implicit memory for performing learned skills and tasks.

 memory stores information about motor skills and procedures such as riding a bicycle, using a
software program, or cooking your favorite meal.
 Semantic and
episodic memories are grouped together as declarative memories. These types of memories are
declarative in the sense that they can easily be described in words, or “declared.” In contrast, procedural
memories are often quite difficult to describe verbally but are easy to demonstrate or perform. Declarative
memories are typically recalled consciously or explicitly, whereas procedural memories are usually
recalled unconsciously or implicitly. Learning a skill, such as driving a car, requires quite a bit of
attention and conscious effort. Once mastered, however, a skill such as driving can become quite
automatic. In addition to procedural memories, classical conditioning, habituation, and sensitization are
also considered examples of nondeclarative or implicit processes.

PARTS OF THE BRAIN SUPPORTING LEANING AND MEMORY

Cerebellum in classical conditioning (Purkinje Cells)

 James Albus (1971) suggested learning will occur if the climbing-fiber and parallel-fiber
synapses onto a Purkinje cell are activated at the same time.
 Ito recorded EPSPs in the Purkinje cells in response to electrical stimulation of the parallel fibers.
Subsequently, both climbing and parallel fibers were simultaneously stimulated. The paired
stimulation produced a reduction in Purkinje cell EPSPs that lasted up to one hour. The reduced
activity in the Purkinje cells is known as long-term depression, or LTD.
 the cerebellum (skeletal reflexes). In addition to the cerebellum, trace conditioning requires
activity in the forebrain.
Amygdala (Classical Conditioning of Fear)

 Many emotional responses to environmental stimuli are learned by the process of classical
conditioning.
 Plays an important role in the classical conditioning of emotional responses
Temporal Lobe (Declarative Memory)

 Significant evidence of the temporal lobe’s involvement in memory came from case studies of
patients with anterograde amnesia.
 Patients suffering from anterograde amnesia appear to retain their newly acquired procedural,
implicit memories while experiencing a dramatic deficit in their ability to form new explicit
memories.
  Studied cases of anterograde amnesia is a man known in the literature only as patient H. M.
Broca’s Area (Semantic Memory)
Medial occipital Lobe (Semantic Memory)
Premotor Area (Semantic Memory)
Prefrontal Cortex (Short-term memory)
Basal Ganglia (Procedural memory)

Long-Term Potentiation (LTP) Beginning in the 1970s, researchers began to investigate neural
mechanisms in the hippocampus that appear to provide a basis for learning and memory.

The major

anatomical features of the hippocampus and surrounding structures

 - Ventral to the hippocampus are the parahippocampal cortex and the rhinal cortex.
- Input from the association areas of the cortex enters the parahippocampal and rhinal cortices,
which in turn transmit the information to the hippocampus.
- The pathways connecting the hippocampus to the rest of the brain, as well as the connections
formed within the hippocampus itself, are also central to our understanding of the functions of
this structure.
Parahippocampal cortex

 An area of cortex just ventral to the hippocampus.

Rhinal cortex

 An area of cortex ventral to the hippocampus.

 There is subdivision of the rhinal cortex which are entorhinal and perirhinal cortices.
Entorhinal cortex

 A subdivision of the rhinal cortex, which lies ventral to the hippocampus.

Perirhinal cortex

 A substructure of the rhinal cortex.

Fornix

 A pathway carrying information from the hippocampus to the hypothalamus.

 Output from the area generally travels along the fornix, a pathway that terminates in the
hypothalamus.
Ammon’s horn

 One of two major layers of neurons found in the hippocampus.

 divided into four sections, named CA1 to CA4. (CA stands for the Latin term for Ammon’s horn,
cornu Ammonis.)
Dentate gyrus

 One of two major layers of neurons found in the hippocampus.

Perforant pathway

 A pathway made up of axons originating in the rhinal cortex that form synapses in the dentate
gyrus of the hippocampus.
 Input from the rhinal cortex travels along the perforant pathway, whose axons form synapses on
the cells of the dentate gyrus.
Mossy fiber (hippocampus)

 An axon from the dentate gyrus that synapses on cells found in CA3 of Ammon’s horn.
 Axons from the dentate gyrus, also known as mossy fibers, synapse on cells found in CA3 (the
third division of Ammon’s horn). Axons from CA3 form two branches.
Schaffer collateral pathway
  A pathway connecting CA3 to CA1 in Ammon’s horn of the hippocampus.
 Axons from CA3 form two branches. One branch, the Schaffer collateral pathway, synapses with
the cells of CA1. The other branch exits the hippocampus as the fornix.
Long-Term Potentiation (LTP)

 The application of a rapid series of electrical shocks to an input pathway increases the
postsynaptic potentials recorded in target neurons
 The change in responsiveness in the target cells after the rapid series of shocks is known as long-
term potentiation, or LTP.
 The fact that LTP lasts a long time is important because we believe that some memories last
throughout life. Second, it takes only seconds of input to produce LTP.
 Both the Hebbian synapse and LTP require relatively simultaneous firing, or associativity, in the
pre- and postsynaptic neurons.
 strengthened. LTP also requires cooperativity, which means that several synapses onto the target
postsynaptic neuron must be simultaneously active.
 LTP appears to be a general process of learning that “can be implemented by a variety of
receptors and signaling systems”
Cooperativity

 Nearly simultaneous stimulation by two or more axons produces LTP much more strongly than
does repeated stimulation by just one axon.
 A condition for the formation of LTP in which several synapses onto the target postsynaptic
neuron must be simultaneously active.
Associativity

 Pairing a weak input with a strong input enhances later response to the weak input
 A condition believed necessary for learning in which the pre- and postsynaptic neurons are nearly
simultaneously active.

Illustration 1: AMPA and NMDA Synapses (two types of glutamate receptor)

Illustration 2: AMPA and NMDA Synapses (two types of glutamate receptor)

The AMPA receptor is excited by the neurotransmitter glutamate, but it can also respond to a drug

called a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (abbreviated AMPA). The NMDA receptor

is also ordinarily excited only by glutamate, but it can respond to a drug called N-methyl-D-aspartate
(abbreviated NMDA). NMDA glutamate receptors, illustrated in Figure 12.18, are particularly well-suited
to facilitate both associativity and cooperativity. For glutamate from a presynaptic neuron to influence
postsynaptic NMDA receptors, both neurons must be simultaneously active (associativity). The channel
of the NMDA receptor is normally blocked by a molecule of magnesium (Mg2+). Depolarization of the
postsynaptic cell acts to expel the Mg2+ from the channel. This depolarization typically requires the
activity of other synapses onto the same postsynaptic neuron (cooperativity). When a molecule of
glutamate is bound to the now unblocked receptor, both sodium (Na+) and calcium (Ca2+) enter the cell.
The entrance of Ca2+ stimulates several second messengers within the cell, which initiate the structural
changes necessary to strengthen the synapse.

Improving Memory

 Stimulant Drugs
 Emotionally Stimulating Experiences
 Cortisol
 Ginkgo biloba (Debatable)
 Bacopa monnieri (Debatable)
 Rehearsal
 Physical Exercise

DISORDERS
Anterograde Amnesia

 Inability to form memories for events that happened after brain damage
 patients have good recall for events that occurred prior to the time of their brain damage, but they
seem unable to remember anything they experience following their brain damage.
Retrograde Amnesia

 loss of memory for events that occurred before the brain damage
Korsakoff’s Syndrome

 is brain damage caused by prolonged thiamine deficiency due to consumption of large amounts of
alcohol
Alzheimer’s Disease

 the most common type of dementia. It is a progressive disease beginning with mild memory loss
and possibly leading to loss of the ability to carry on a conversation and respond to the
environment.

BRAIN DAMAGE
Brain Tumors

 Tumor or neoplasm (new growth) is a mass of cells that grows independently of the rest of the
body
Encapsulated Tumors

 almost always benign

Meningiomas

 tumors that grow in meninges

 20 percent are found in the human brain
Infiltrating Tumors

 Usually malignant
Gliomas

 tumors that develop from glial cells

Metastatic Tumors

 tumors that grow from infiltrating cells that are carried to the brain by the blood
stream

Stroke
  Sudden onset cerebrovascular disorders that cause brain damage
Cerebral Hemorrhage

 Bleeding in the brain

 Occurs when a cerebral blood vessel ruptures and blood seeps into the surrounding
tissue and damages it
Aneurysm

 an abnormal swelling or bulge in the wall of a blood vessel, such as an artery

Cerebral Ischemia

 Disruption of the blood supply to an area of the brain

Causes
 Thrombosis
 Embolism
 Arteriosclerosis

Traumatic Brain Injuries

 Blow to the head that can cause confusion, sensorimotor disturbances, or loss of consciousness
Closed-Head TBIs

 brain injuries produced by blows that do not penetrate the skull

Contusions

 involve damage to the cerebral circulatory system

Mild TBI (formerly concussions)

 when there is a disturbance of consciousness following a blow to the head and there
is no evidence of contusion

Brain Infections

 An invasion of the brain by microorganisms and the resulting infection is called encephalitis
Bacterial Infections

 Can lead to the formation of cerebral abscesses (pockets of pus in the brain)
Meningitis
Syphilis

 passed from infected to noninfected individuals through contact with genital sores

General Paresis
  syndrome of mental illness and dementia
Viral Infections
◦ Rabies
◦ Mumps
◦ Herpes

NEUROTOXINS

 Toxic chemicals that can enter general circulation from the gastrointestinal tract, from the lungs,
or through the skin
Mercury or Lead

 toxic psychosis
 Drugs with lead content
Tardive dyskinesia

 involuntary smacking and sucking movements of the lips, thrusting and rolling of the
tongue, lateral jaw movements, and puffing of the cheeks

Neurological Diseases DISEASES ASSOCIATED WITH BRAIN DAMAGE

Epilepsy

 Seizures are repeatedly generated by brain dysfunction

 Convulsions (motor seizures), tremors (clonus), rigidity (tonus), and loss of both balance and
consciousness
Focal Seizures

 seizure that does not involve the entire brain

Simple (Jacksonian Seizures)
 symptoms are primarily sensory or motor or both
Complex (Temporal Lobe Epilepsy)
 begin in the temporal lobes. Patient engages in compulsive, repetitive, simple
behaviors - automatisms
Generalized Seizures

 involve the entire brain

Tonic - clonic seizure
 loss of consciousness, loss of equilibrium, and violent tonic- clonic convulsion
Absence seizure
  vacant look, fluttering eyelids

Parkinson’s Disease
Movement disorder

 Tremors during inactivity, muscular rigidity, difficulty initiating movement, slowness of

movement and a masklike face.
Severe degeneration in the substantia nigra
nigrostriatal pathway
o originating in the substantia nigra and projecting to the basal ganglia.

Undersupply of dopamine
o treatment is L-dopa

Huntington’s Disease

 Progressive motor disorder

 Simple genetic basis (dominant gene:huntingtin) and associated with severedementia
 First clinical sign: increased fidgetiness
 As the disorder develops: rapid, complex, jerky movements of entire limbs,psychiatric symptoms
and cognitive deficits

Multiple Sclerosis

 Progressive disease that attacks the myelin of axons in the CNS

 Often considered to be an autoimmune disorder
 Symptoms include: visual disturbances, muscular weakness, numbness, tremor, ataxia (loss of
motor coordination)
 Risk factors: Vitamin D deficiency, viral infections, and cigarette smoking