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40 Cards in this Set

  • Front
  • Back

major depression

-definining feature: loss of pleasure


-anhedonia


-guilt & grief


-delusional thinking


-psychomotor retardation


-elevated glucocorticoid levels, smaller hippocampus,

anhedonia

-inability to feel pleasure


-also called dysphoria


-consistent among depressives

Aaron Beck

-considered depression to be primarily a disorder of thought rather than emotion


-depressives tend to see the world in a distorted, negative way

psychomotor retardation

-person moves & speaks slowly


-everything requires tremendous effort and concentration


-severely, profoundly depressed people rarely attempt suicide (not enough energy to do so)

effects of glucocortioicds

-problems with hippocampal-dependent (declarative) memory


-can deplete dopamine from pathway & effect other 2 neurotransmitters


-can suppress immune system


-increased risk of osteoporosis & heart disease


-smaller frontal cortex

unipolar depression

-fluctuates from feeling extremely depressed to feeling reasonably normal

bipolar depression

-fluctuates between deep depression and wild, disorganized hyperactivity


-also called manic depression

seasonal affective disorder (SAD)

-rhythm of depression symptoms is annual


-sufferers get depressed during winter


-retinal cells send average amount of light to limbic system

3 neurotransmitters involved in depression

-norepinephrine


-serotonin


-dopamine

tricyclics

-class of antidepressants that stop the repute of neurotransmitters


-neurotransmitter remains in synapse longer


-work on all 3 neurotransmitters

MAO inhibitors

-class of antidepressants that block the degradation of neurotransmitters in the synapse by inhibiting the action of monoamine oxidase


-work on all 3 neurotransmitters

timing of depression

-it takes anti-depressants much longer to work for depressed people


-theory 1: too much neurotransmitters; cell stops listening and down regulates the number of receptors for the neurotransmitter to decrease its sensitivity to that messenger


-theory 2: not enough neurotransmitters; post-synaptic cells shut off some of the receptors to neurotransmitters; serve as feedback signal to decide how much more neurotransmitters should be released; auto receptors on the first neuron will down-regulate more than receptors on the second

electroconvulsive therapy (ECT)

-reduces norepinephrine auto-receptors


-person feels immediately better; leads to down-regulation

serotonin

-involved in incessant ideation and ruminating thoughts


-SSRIs effective on people with OCD


-obsessive sense of doom, failure, and despair


-many different subtypes of receptors

norepinephrine

-locus ceruleus sprays all over brain to wake up cortex


-lowers threshold so you respond faster


-makes you more alert


-not enough in depression (psychomotor retardation)

dopamine

-pleasure pathway


-the more addictive it is, the more it hits the dopamine system


-lack of amount in depression (dysphoria)

substance P

-plays a role in pain perception


-tells brain that there's pain through spinal cord


-drugs that block substance P work as anti-depressants


limbic system

-motivation


-emotion

hypothalamus

-regulates process like breathing and heart rate

cortex

-abstract cognition & imagination


-tells depressed people negative thoughts


-cortex thinks abstract negative thought and convinces the rest of the brain that it's as real as a physical stressor

cingulotomy

-on people with vastly crippling depressions that are resistant to drugs, ECT or therapy


-disconnects anterior cingulate cortex (ACC) from rest of brain

anterior cingulate cortex (ACC)

-emotional component of pain


-feelings about pain and negative emotions


-associated with extreme negative emotions and sorrow


-also associated with social neglect & isolation


-overactive in depression; almost always activated (constant negative thoughts)


-neurons respond to pain of all sorts

amygdala

-hyperactive in depressives


-usually activated with fear in depression, no change when they see fear; instead, way more active to sadness

prefrontal cortex (PFC)

-highly responsive to mood


-lateralization in brain


-right: negative emotions


-left: positive emotions


-in depression: decreased left PFC activity and elevated right PFC activity

factors that affect depression

-neurochemistry


-neuroanatomy


-genetics


-immunology


-endocrinology

genetics & depression

-the more closely related two individuals are, the more genes they share in common and the more likely they are to share a depressive trait


-the more genes people share within a family, the more environment they share as well

immunology & depression

-chronic illness that involves over activation of immune system is more likely to cause depression than other equally severe and prolonged illnesses that don't involve the immune system

cytokines

-act as messengers between immune cells


-can stimulate CRH release, which increases ACTH and glucocorticoids


-can cause depression


-also interacts with dopamine, serotonin, & norepinephrine

thyroid

-releases hormones of growth, metabolism, & reproduciton


-depression: too little thyroid hormone


(secondary to thyroid problem; need meds for theyroid, not depression)

women & depression

-women are more likely to be diagnosed with unipolar depression


-in bipolar depression, they have more depressive symptoms


-particularly at risk at certain reproductive points: menstruation, menopause, and after childbirth (estrogen & progesterone)


stress & depression

1. stress generation: people who are prone to depression tend to experience stressors at a higher rate


2. people who are undergoing a lot of life stressors ar more likely to have major depression

reasons for female bias

1. female psychological orientation of rumination


2. psychosocial (women do not have as much control)


3. change in estrogen or progesterone

atypical depression

-dominated by psychomotor features of disease (incapacitating physical & psychological exhaustion)


-lower than normal glucocorticoid levels


feedback resistance

-cause of excessive secretion of glucocoritoicds in stress response


-brain is less effective than it should be at shutting down glucocorticoid secretion


-in depressives, feedback regulation fails


-brain does not sense feedback signals

DHEA

-hormone that has the ability to block glucocorticoid receptors in brain


-inhibits glucocorticoids


-encourages neurogenesis


-anti-depressant qualities


-gets less as we get older


abortion pill

-blocks glucocorticoid receptors


-anti-depressant effect

learned helpnessness

-no chance at escaping and no prediction of event occurring


-will not take opportunities given to them


-learned to do nothing and lose motivation


-humans in depression


-rats have higher risk of cancer

internalized locus of control

-belief that they were the masters of their own destiny and had a great deal of control in their lives


-the more likely that someone has an internal locus of control, the less likelihood of a depression

externalized locus of control

-tended to attribute outcomes to chance and luck


-far more vulnerable to learned helplessness


-more at risk for depression

5-HTT

-serotonin-transporter


-pump that causes the reuptake of serotonin from the synapse


-different allelic versions differ as to how good they are at removing serotonin from the synapse


-glucocorticoids help regulate how much 5-HTT gene you have


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