CHAPTER 17: EMOTION, STRESS, AND HEALTH

BRAIN MECHNISMS IN HUMAN EMOTION is more pronounced there—which implies right-hemisphere

dominance for facial expressions
I. Cognitive Neuroscience of Emotion
a. Brain activity associated with each human emotion is diffuse—there V. Neural Mechanisms of Human Emotion: Current Perspectives
is not a center for each emotion a. Emotional situations produce widespread increases in
b. There is virtually always activity in motor and sensory cortices when cerebral activity, not just in the amygdalae and prefrontal
a person experiences an emotion or empathizes with a person cortex.
experiencing an emotion b. All brain areas activated by emotional stimuli are also activated
i. embodiment of emotions: re-experiencing of related during other psychological processes.
patterns of motor, autonomic, and sensory neural activity c. No brain structure has been invariably linked to a particular
during emotional experiences emotion.
c. Similar patterns of brain activity tend to be recorded when a person d. The same emotional stimuli often activate different areas in
experiences an emotion, imagines that emotion, or sees somebody different people.
else experience that emotion
STRESS AND HEALTH
II. Amygdala and Human Emotion
a. Responds to fear and other emotions  Stress (Response): a cluster of physiological changes when the body is exposed
b. performance of any task with an emotional component to harm or threat
c. evaluating the emotional significance of situations.  All stressors produce the same core pattern of physiological changes, whether
d. Urban-Wiethe Disease: genetic disorder that often results in psychological or physical
calcification (hardening by conversion to calcium carbonate, the main  chronic psychological stress that has been most frequently implicated in ill
component of bone) of the amygdala and surrounding anterior medial health
temporal-lobe structures in both hemispheres
i. Lose the ability to recognize facial expressions of fear I. The Stress Response
ii. cannot describe fear-inducing situations or produce fearful
expressions  Selye:
iii. sometimes have difficulty recognizing other complex visual o Dual Nature
stimuli  Short Term: adaptive response to stressor
 Long Term: maladaptive changes (eg. enlarged adrenal glands)
III. Medial Prefrontal Lobes and Human Emotion o Stress Response due to
a. Emotion and cognition: components of the same system activation of anterior-pituitary
b. medial prefrontal lobes (including the medial orbitofrontal cortex adrenal-cortex system
and anterior cingulate cortex) are the sites of emotion–cognition  Stressors acting on
interaction that have received the most attention neural circuits 
c. evidence of activity in the medial prefrontal lobes when emotional anterior pituitary
reactions are being cognitively suppressed or re-evaluated releases ACTH
i. suppression paradigms: participants are directed to inhibit (adrenocorticotropic
their emotional reactions to unpleasant films or pictures hormone)  adrenal
ii. reappraisal paradigms: participants are instructed to cortex releases
reinterpret a picture to change their emotional reaction to it. glucocorticoids
d. FUNCTIONS: (produces components
i. monitor the difference between outcome and expectancy of stress response)
ii. encode stimulus value over time  Level of glucocorticoids:
iii. predict likelihood of error measure of stress
iv. mediate the conscious awareness of emotional stimuli o Ignored contributions of
e. Neurons of the ACC: negative emotional reactions; neurons sympathetic NS
directly involved in emotional processing appear to be sparse and  Stressors  activate
widely distributed in the human medial prefrontal lobes sympathetic NS 
adrenal medulla
IV. Lateralization of Emotion increases epinephrine &
a. Lateralization: left and right cerebral hemispheres are norepinephrine
specialized to perform different emotional functions  Asserts that both physical and psychological stressors induce the same
b. PROMINENT THEORIES general stress response  partly correct (all kinds of common
i. The right-hemisphere model of the cerebral psychological stressors act like physical stressors)
lateralization of emotion holds that the right
hemisphere is specialized for all aspects of  1990s: stressors produce physiological reactions that participate in the
emotional processing: perception, expression, and body’s inflammatory responses.
experience of emotion. o stressors increase cytokines (major stress hormones; cause
ii. The valence model proposes that the right inflammation/fever) levels in the blood
hemisphere is specialized for processing negative
emotion and the left hemisphere is specialized for II. Animal Models of Stress
processing positive emotion. [R- | L+]  2 Problems:
c. Overall comparisons between left and right hemispheres o Ethics
revealed no interhemispheric differences in either the amount o Are often of questionable scientific value: difficult to relate to common human
of emotional processing or the valence of the emotions being stressors
processed.  Conspecifics- members of the same species, involve the study of social threat,
d. However, on a structure-by-structure basis, some kinds of male mammals
emotional processing were lateralized to the left hemisphere  Subordination Stress- when conspecific threat becomes an enduring feature of
in certain structures and to the right in others daily life  becomes bullying in humans
i. lateralization in the amygdalae—more activity is
often observed in the left amygdala III. Psychosomatic Disorders: The Case of Gastric Ulcers
e. Asymmetry of facial expressions: each facial expression  Psychosomatic Disorders: medial disorders in which psychological factors pay
begins on the left side of the face and, when fully expressed, a causal role
 gastric ulcers- painful lesions to the lining of the stomach and duodenum
 CHAPTER 17: EMOTION, STRESS, AND HEALTH
o believed to have been caused by Helicobacter pylori (i.e., H. pylori; also
present In healthy individuals) except those caused by nonsteroidal anti-
inflammatory agents such as aspirin
o caused by H. pylori + stress
IV. Psychoneuroimmunology: Stress, the Immune System, and the Brain
 Psychoneuroimmunology: the study of interactions among
psychological factors, the nervous system, and the immune system.
 4 Lines of Defense
o Behavioral Immune System: eg. avoiding contact with sick
people, bodies are primed to respond more aggressively to infection
when they perceive signs of infection in other
o Surface Barriers: skin, coughing, sneezing, tears, mucous, and
numerous chemical barriers.
o Innate Immune System: first component of the immune system to
react
 Triggered when toll-like receptors bind to molecules on the
surface of the pathogens or when injured cells send out
alarm signals
 Inflammation: triggered by the release of chemicals from
damaged cells
 Cytokines- attract leukocytes and other phagocytes,
promote healing of damaged tissue one pathogens
are destroyed
o Microglia & Phagocytes: specific to CNS\
o Phagocytosis
o Adaptive Immune System:
 is slower; its immune reaction to pathogens takes longer to
be fully manifested.
 is specific: that it reacts against specific antigens.
 has a memory; once it has reacted against a particular
pathogen, it reacts more effectively against that same
pathogen in the future.
 gives vaccinations their prophylactic (preventive) effect
 vaccination: injecting weakened form of virus
 immunization: process of creating immunity through
vaccination
 Lymphocytes: produced in bone marrow and thymus gland,
stored in the lymphatic system
 T Cells: cell-mediated immunity
o Phagocyte ingests foreign microorganism
o Phagocyte displays the microorg’s antigen
(molecules, usually proteins, that can trigger an
immune response) on the surface of its cell
membrane  display attracts T cells
o T cell has two kinds of receptors on its surface, one
for molecules that are normally found on the
surface of phagocytes and other body cells, and
one for a specific foreign antigen
o Once a T cell with a receptor for the foreign antigen
binds to the surface of an infected macrophage, a
series of reactions is initiated (eg. multiplication of
the bound T cell, creating more T cells with the
specific receptor necessary to destroy all invaders
that contain the target antigens and all body cells
that have been infected by the invaders.
 B Cells: antibody-mediated immunity
o B cell binds to a foreign antigen for which it contains
an appropriate receptor.
o B cell multiplies and synthesizes and releases
antibodies into the intracellular fluid, where they
bind to the foreign antigens and destroy or
deactivate the microorganisms that possess them
o Memory B cells have a long life and accelerate
antibody-mediated immunity if there is a
subsequent infection by the same microorganism.
o Stress and the Immune System
 Effects of stress on immune function depended on the kind of
stress (Segerstro & Miller, 2004)
 Acute (brief: >100 mins.) stressors: improve innate immune
system
 Chronic stressors: damage adaptive immune system
 Distress: disrupts health & functioning
 Eustress: improves health & functioning
 Bidirectional role of cytokines in the innate immune system
o Short-term cytokine-induced inflammatory responses help the
body combat infection,
o Long-term cytokine release is associated with a variety of
adverse health consequences
 How stress influences immune function
o Stress affects the anterior-pituitary adrenal-cortex system and
the sympathetic-nervous- system adrenal-medulla system 
affects immune fxn
o T and B Cells: have receptors for glucocorticoids (APAC)
o Lymphocytes: have receptors for epinephrine, norepinephrine,
and glucocorticoids (APAC, SNS-AMS)
o Cytokines: produced by cells in the NS and the immune sys
 3 reasons why stress-produced decreases in immune function may
not be reflected in an increased susceptibility to infectious disease:
o The immune system seems to have many redundant components;
thus, disruption of one of them may have little or no effect on
vulnerability to infection.
o Stress-produced changes in immune function may be too
short-lived to have substantial effects on the probability of
infection.
o Declines in some aspects of immune function may induce
compensatory increases in others.
V. Early Experience of Stress
 early exposure to stress often increases the intensity of subsequent stress
responses (e.g., increases the release of glucocorticoids in response to
stressors)
 As adults, rats that had been handled as pups displayed smaller increases
in circulating glucocorticoids in response to stressors
 Salutary (health-promoting) effects of the early handling resulted from the
extra grooming, rather than from the handling itself
 Rats that are separated from their mothers in infancy display elevated
behavioral and hormonal responses to stress as adults.
VI. Stress and the Hippocampus
 Hippocampus susceptible to stress perhaps because of its particularly
dense population of glucocorticoid receptors
 Effects of Stress in the Hippocampus
o reduce dendritic branching
o reduce adult neurogenesis
o modify the structure of some hippocampal synapses
o disrupt the performance of hippocampus-dependent tasks
 Effects of stress on the hippocampus appear to be mediated by elevated
glucocorticoid levels:
o Induced by corticosterone (a major glucocorticoid)
o Blocked by adrenalectomy (surgical removal of the adrenal glands)