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Week 4 reading: Taming Stress
Out of Balance:
•A stressor is anything in the environment that knocks the body out of homeostasis, and the stress
response is the array of physiological adaptations that ultimately re-establishes balance.
•The response principally includes the secretion of two types of hormones from the adrenal
glands: epinephrine, also known as adrenaline, and glucocorticoids.
In humans, the relevant glucocorticoid is called cortisol, also known as hydrocortisone.
•Epinephrine and glucocorticoids mobilize energy for muscles, increase cardiovascular tone so
oxygen can travel more quickly, and turn off nonessential activities like growth.
The hormones work at different speeds.
-In a fight-or-flight scenario, epinephrine is the one handing out guns; glucocorticoids are the
ones drawing up blueprints for new aircraft carriers needed for the war effort.
Primates have it tough, however.
- More so than in other species, the primate stress response can be set in motion not only by a
concrete event but by mere anticipation.
•When this assessment is accurate (“This is a dark, abandoned street, so I should prepare to run”),
an anticipatory stress response can be highly adaptive.
But when primates, human or otherwise, chronically and erroneously believe that a homeostatic
challenge is about to come, they have entered the realm of neurosis, anxiety and paranoia.
•In the 1950s and 1960s pioneers such as John Mason, Seymour Levine and Jay Weiss began to
identify key facets of psychological stress.
They found that such stress is exacerbated if there is no outlet for frustration, no sense of control,
no social support and no impression that something better will follow.
-Thus, a rat will be less likely to develop an ulcer in response to a series of electric shocks if it
can gnaw on a bar of wood throughout, because it has an outlet for frustration.
-A baboon will secrete fewer stress hormones in response to frequent fighting if the aggression
results in a rise, rather than a fall, in the dominance hierarchy; he has a perception that life is
-A person will become less hypertensive when exposed to painfully loud noise if she believes she
can press a button at any time to lower the volume; she has a sense of control.
•Suppose such buffers are not available and the stress is chronic.
Repeated challenges may demand repeated bursts of vigilance.
At some point, this vigilance may become overgeneralized, leading an individual to conclude
that he must always be on guard—even in the absence of the stress.
-And thus the realm of anxiety is entered.
Alternatively, the chronic stress may be insurmountable, giving rise to feelings of helplessness.
*Again this response may become overgeneralized: a person may begin to feel she is always at a
loss, even in circumstances that she can actually master.
Stress and Anxiety:
•One structure is primarily affected: the amygdala, which is involved in the perception of and
response to fear-evoking stimuli.
Interestingly, the amygdala is also central to aggression, underlining the fact that aggression can
be rooted in fear—an observation that can explain much sociopolitical behavior.
•To carry out its role in sensing threat, the amygdala receives input from neurons in the outermost
layer of the brain, the cortex, where much high-level processing takes place.
Some of this input comes from parts of the cortex that process sensory information, including
specialized areas that recognize individual faces, as well as from the frontal cortex, which is
involved in abstract associations.
-In the realm of anxiety, an example of such an association might be grouping a gun, a hijacked
plane and an anthrax-tainted envelope in the same category.
•The sight of a fire or a menacing face can activate the amygdala—as can a purely abstract
•The amygdala also takes in sensory information that bypasses the cortex.
As a result, a subliminal preconscious menace can activate the amygdala, even before there is
conscious awareness of the trigger.
Ex. Imagine a victim of a traumatic experience who, in a crowd of happy, talking people,
suddenly finds herself anxious, her heart racing. It takes her moments to realize that a man
conversing behind her has a voice similar to that of the man who once assaulted her. The
amygdala, in turn, contacts an array of brain regions, making heavy use of a neurotransmitter
called corticotropin-releasing hormone (CRH).
• One set of nerve cells projecting from the amygdala reaches evolutionarily ancient parts of the
midbrain and brain stem.
These structures control the autonomic nervous system, the network of nerve cells projecting to
parts of the body over which you normally have no conscious control (your heart, for example).
One half of the autonomic nervous system is the sympathetic nervous system, which mediates
“fight or flight.”
Activate your amygdala with a threat, and soon the sympathetic nervous system has directed
your adrenal glands to secrete epinephrine.
-Your heart is racing, your breathing is shallow, your senses are sharpened.
•The amygdala also sends information back to the frontal cortex.
In addition to processing abstract associations, the frontal cortex helps to make judgments about
incoming information and initiating behaviors based on those assessments.
-So it is no surprise that the decisions we make can be so readily influenced by our emotions.
•Moreover, the amygdala sends projections to the sensory cortices as well, which may explain, in
part, why sensations seem so vivid when we are in certain emotional states—or perhaps why
sensory memories (flashbacks) occur in victims of trauma.
•There are two general forms of memory.
1) Declarative, or explicit, memory governs the recollection of facts, events or associations.
2) Implicit memory has several roles as well.
It includes procedural memory: recalling how to ride a bike or play a passage on the piano.
And it is involved in fear.
* Remember the woman reacting to the similarity between two voices without being aware of it.
-In that case, the activation of the amygdala and the sympathetic nervous system reflects a form
of implicit memory that does not require conscious awareness.
•Researchers have begun to understand how these fearful memories are formed and how they can
be overgeneralized after repeated stress.
The foundation for these insights came from work on declarative memory, which is most likely
situated in a part of the brain called the hippocampus.
-Memory is established when certain sets of nerve cells communicate with one another
-Such communication entails the release of neurotransmitters—chemical messengers that travel
across synapses, the spaces between neurons.
Repeated stimulation of sets of neurons causes the communication across synapses to be
strengthened, a condition called long-term potentiation (LTP).
•As will become quite pertinent when we turn to depression, glucocorticoid exposure can impair
LTP in the hippocampus and can even cause atrophy of neurons there.
This phenomenon constitutes the opposite of the stress response in the amygdala.
Severe stress can harm the hippocampus, preventing the consolidation of a conscious, explicit
memory of the event; at the same time, new neuronal branches and enhanced LTP facilitate the
amygdala’s implicit memory machinery.
-In subsequent situations, the amygdala might respond to preconscious information—but
conscious awareness or memory may never follow.
*According to LeDoux, such a mechanism could underlie forms of free-floating anxiety.
•The amygdala’s perception of stress ultimately leads to the secretion of epinephrine and
The glucocorticoids then activate a brain region called the locus coeruleus.
-This structure, in turn, sends a powerfully activating projection back to the amygdala, making
use of a neurotransmitter called norepinephrine (a close relative of epinephrine).
The amygdala then sends out more CRH, which leads to the secretion of more glucocorticoids.
•The medicines that already exist do target aspects of the stress system.
The minor tranquilizers, such as Valium and Librium, are in a class of compounds called
-They work in part by relaxing muscles; they also inhibit the excitatory projection from the locus
coeruleus into the amygdala, thereby decreasing the likelihood that the amygdala will mobilize
the sympathetic nervous system.