antidepressants - dr austin

4 hours : 20 questions

list the executive and behavioral depression symptoms

• anhedonia

  • don’t enjoy things like before

• avolition

  • lack of goal-directed behavior

• apathy

  • lack of interest

• lethargy

  • change in energy levels

• cognitive

  • slowed thinking, poor memory, difficulty concentrating

list the affective depression symptoms

• sadness

• anxiety

• guilt

• worthlessness

• disgust with self

• thoughts of self-harm

• catharsis of self-destruction

what is the hippocampus responsible for?

what is it’s effect on depression?

forming and storage of associative and episodic memories

depression: misinterpreting episodes, looking backwards at “embarrassing moments”

list structural changes of the brain in depression

reduced neuronal density

dendritic atrophy

associations with HPA axis activation

decr. brain-derived neurotrophic factor (BDNF)

what parts of the brain will have inappropriae or exaggerated responses?

• amygdala

• anterior cingulate cortex (ACC)

• hippocampus

where in the brain do you see decreased connectivity?

prefrontal cortex (PFC)

hippocampus

in terms of activity changes in the brain, what is important to look at?

changes from baseline!!!!!

response to stress —> like when you’re sick you’re in a bad mood

where do most monoamine neurons (serotonergic, dopaminergic, noradrenergic) originate in?

where do they project to?

originate: midbrain or brainstem

project to entire brain

what is the monoamine hypothesis?

it’s the most popular hypothesis

depression pathology is associated with decreased activity of monoamines (serotonin, dopamine, and norepinephrine) in the CNS

T/F almost every substance that increases levels of monoamines in synapse has antidepressant properties

TRUE — monoamine hypothesis

T/F stimulation of MAO improves mood

FALSE — inhibition of MAO improves mood

makes sense because monoamine oxidase degrades the monoamines, and monoamines improve mood

what is a major component of evidence AGAINST the monoamine hypothesis?

only 50-70% of pts experience full response to therapies that target monoamines

basically we’re missing a causal connection

why does reserpine cause depression?

blocks VMAT —> reduces vesicular storage of monamines

_______ abnormalities are seen in some MDD patients

HPA-axis —> incr. cortisol levels

what is “sickness behavior”?

may produce depression-like symptoms

association of increased levels of pro-inflammatory mediators

-enhance HPA activation and impair serotonergic activity

left off on slide 13