Psyc121 Final – Flashcards
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Stage 2
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adaptation: During this stage, if the stress continues, the body adapts to the stressors. Changes at many levels take place in order to reduce the effect of the stressor.
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Stage 3
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exhaustion: The body's resistance to the stress may gradually be reduced, or may collapse altogether
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Homeostasis
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tendency toward a relatively stable equilibrium between interdependent elements, especially as maintained by physiological processes Deviations from homeostasis often require a vigorous response to attempt to restore homeostasis
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Hypothalamic-pituitary-adrenal axis (HPA axis)
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H - hypothalamus (CRF) P - pituitary (ACTH) A - adrenal (Corticosterone or Cortisol) It helps regulate things such as your temperature, digestion, immune system, mood, sexuality and energy usage. It's also a major part of the system that controls your reaction to stress *helps maintain homeostasis*
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Glucocorticoids
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like cortisol in your blood, they help to release stores of energy from fat They also INHIBIT the HPA axis *secreted especially in times of stress*
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(Review) Effects of glucocorticoids
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Very stressed ppl may have deficits in hypothalamus or too much pumping of adrenal cortex ? *Glucocorticoids = secreted in times of stress, so they: Interfere with memory & Promotes fear/ anxiety*
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Effects of cortisol
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stimulates the synthesis of glucose inhibits the uptake of glucose into fat and muscle stimulates the breakdown of fat suppresses the immune system can affect behavior like fear and learning and memory reduces plasma levels of sex steroid hormones *almost (if not all) cells have receptors for cortisol*
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Glucocorticoids & conditioned fear
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Corticosterone given immediately after tone and shock pairing in rats enhances conditioned fear Corticosterone dose-dependently enhances freezing (reduces movement)
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(Review) NBQX
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glutamate antagonist (GABA=glutamate agonist) blocks excitatory effects of glutamate
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Epinephrine
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effects: Increased blood flow to muscles Increased heart rate Rise in blood sugar Piloerection (goosebumps) Stress activates autonomic nervous system to release epinephrine
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Corticotropin releasing factor (CRF) & Neuropinephrine (NE)
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neurotransmitters that act centrally in response to stress
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CRF
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*Increases anxiety* *Enhances conditioned fear* Increases arousal Decreases body weight Interferes with sexual behavior Disrupts sleep
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Long-term stress effects
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*Impaired memory* *Immune suppression* Increased blood pressure Damage to muscles Susceptibility to diabetes Infertility Increased inflammatory responses Increased anxiety Susceptibility to depression
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Long-term stress impairs memory (evidence)
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Rats were stressed daily for 21 days & then given training in the Y maze. Stressed rats spent less time in the baited arm at test than did control rats
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Stress and stressor controllability
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Inescapable, but not escapable, shock enhances subsequent conditioned fear Following rats inescapable shock, rats show decrease in escape learning (learned helplessness)
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The role of the dorsal raphe & serotonin in unpredictable & predictable stress
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After inescapable stress, the DRN (dorsal raphe nucleus) is hyper-responsive to subsequent stimuli and releases more 5-HT (serotonin receptor) in target areas, such as the amygdala
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The role of the frontal cortex & serotonin in unpredictable & predictable stress
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If the frontal cortex can tell if stress is controllable, it turns off DRN (serotonin release)
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Exercise & stress resistance
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Exercise prevents the escape deficit produced by inescapable shock Exercise seems to decrease 5-HTC receptors in DRN target areas (*reduces stress*)
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Depression - prevalence
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Depression affects approximately 18 million Americans In any 1 year ~9.5 % of the population suffers from depression 95% of ppl w/ depression have at least 1 symptom of anxiety
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Depression - types
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major depression (mood disorder consisting of unremitting depression or periods of depression that do NOT alternate w/ periods of mania) bipolar disorder (mood disorder characterized by cyclical periods of mania & depression)
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Depression - symptoms
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Persistent sad, anxious, or "empty" mood Feelings of hopelessness, pessimism Feelings of guilt, worthlessness, helplessness Loss of interest or pleasure in hobbies and activities that were once enjoyed Decreased energy, fatigue, being "slowed down" Difficulty concentrating, remembering, making decisions Insomnia, early-morning awakening, or oversleeping Appetite and/or weight loss or overeating and weight gain Thoughts of death or suicide; suicide attempts Restlessness, irritability Persistent physical symptoms that do not respond to treatment
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Depression - drug treatment
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Monoamine oxidase inhibitors (MAOI's) Tricyclic antidepressants Selective serotonin re-uptake inhibitor (SSRI)/ (SNRI) Ketamine
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Monoamine oxidase (MAO's)
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5-HT (serotonin), NE (neropinephrine) & DA (dopamine) NE & DA are Catecholamine's *degrade/ break down catehcolamines & serotonin into inactive forms
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Monoamine oxidase inhibitors (MAOI's)
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Inhibiting MAO increases synaptic levels of NE, DA and 5-HT
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Tricyclic Antidepressants
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Tricyclic's block the reuptake of NE and 5-HT
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Side effects (Tricyclic Antidepressants)
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sedation (histamine), blurred vision, dry mouth and constipation (Ach blockade)
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Selective serotonin re-uptake inhibitors (SSRI)
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SSRI's block the reuptake of 5-HT
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Side effects (SSRI)
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nausea, nervousness, agitation or restlessness, dizziness, reduced sexual desire, drowsiness, insomnia, weight gain or loss, headache
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Tryptophan
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improves depression symptoms by increasing the level of serotonin in the brain *so, tryptophan depletion produces depressive symptoms in remitted depressed individuals*
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Deep Brain Stimulation of the subgenual anterior cingulate cortex (subgenual ACC)
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disrupting focal pathological activity in limbic-cortical circuits using electrical stimulation of the subgenual cingulate white matter can effectively reverse symptoms in otherwise treatment-resistant depression.
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Ketamine
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NMDA glutamate receptor antagonist A single dose of ketamine eliminates depression within an hour and lasts up to 2 weeks. *restores synapses through BDNF (Brain Derived Neurotropihc Factor) and mTOR* In depression, BDNF lessens... w/ ketamine, BDNF goes back up
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Acute Ketamine
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produces rapid reversal of depression & restores normal synaptic function
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The role of synaptic atrophy (death) in depression
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depression (excessive amounts of corticosterone) results in less excitatory synaptic receptors Ketamine = excessive release of glutamate = so ketamine makes more excitatory synaptic receptors (resets back to "normal synapse" with even more excitatory receptors) b/c of BDNF
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How do effective drug treatments suggest what the underlying biological causes of depression might be?
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Depression is some deficit in monoamine (including 5-HT, NE DA)
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Anxiety - prevalence
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Anxiety affects approximately 25 million Americans. 19.5 % of women and 8% of men have an anxiety disorder. Up to 65% of ppl with anxiety become depressed 95% of ppl w/ depression have at least 1 symptom of anxiety
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PTSD & amygdala activity
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Individuals with PTSD show exaggerated amygdala responding to fearful faces
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Amygdala & conditioned fear
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Inactivation of the amygdala interferes with fear but NOT anxiety
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Bed Nucleus of the stria terminalis & anxiety
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Inactivation of the bed nucleus of the stria terminalis (BNST) interferes with anxiety but NOT fear
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Are fear & anxiety the same?
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fear (Amygdala) = predictable & Short-duration stimulus anxiety (BDNF)= unpredictable & Long-duration stimulus Lesions of the BNST are the same, but not the amygdala reduce fear-like responding to: 1. bright lights 2. intracerebroventricular corticotropin-releasing factor 3. uncontrollable shock 4. exposure to predator odor
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Benzodiazepines
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*effective treatments for anxiety enhance the effect of GABA (glutamate agonist), resulting in sedative properties
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SSRI
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*effective treatment for anxiety Drugs that increase serotonin reduce anxiety (but the role of serotonin in anxiety is confusing)
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(Review) acute affect of 5-HT (serotonin)/ SSRI's
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initial effect is anxiety (about 3 days) until the serotonin balances out
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(Review) Choline - guest lecture
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*enhancement of memory* & healthy brain function most important during prenatal phase but also up until around preteen phase (when brain is still developing/ most neural plasticity)
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The term "stress" was coined by
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d. Walter Cannon?--homeostasis/fight or flight a. Hans Seyle?-- stress/GAS
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The general process by which a physiological reaction produced in the body by the perception of aversive or threatening events is referred to as
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e. stress
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Secretion of glucocorticoids results in
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a. reduced plasma levels of sex steroid hormones. b. increased conversion of protein to glucose. c. greater availability of fatty acids as sources of energy. d. increased blood flow
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All of the following occur during a stress response EXCEPT
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a. the parasympathetic branch of the autonomic nervous system is activated
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Hans Selye argued that ill health induced by chronic stress exposure reflects
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c. the prolonged secretion of glucocorticoids
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Which of the following effects of stress would predispose an organism to develop an infectious illness?
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a. inhibition of the immune response
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Episodes of depression are characterized by
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b. extreme sadness
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Which of the following is NOT a symptom of depression?
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c. increased appetite for sex
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A key function of monoamine oxidase is to
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d. degrade catecholamines and serotonin into inactive forms
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Fluoxetine (Prozac) is an effective treatment for ________ that works by ________.
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depression & OCD; blocking serotonin reuptake
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The tricyclic antidepressant drugs are monoamine agonists in that these drug
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a. block the reuptake of norepinephrine and serotonin into the terminals.
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An effective therapy for treatment-resistant depression involves the use of
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e. electrical stimulation of the subgenual ACC.
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The monoamine hypothesis states that depression is caused by
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a. overactivity of monoaminergic neurons.
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