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Block 8 Week 1 Colt > Neurobiology of Depression - Craviso > Flashcards

Neurobiology of Depression - Craviso Flashcards

1
Q

What are the areas of the brain that are involved in depression?

A 
Hypothalamus
Hippocampus
Cingulate gyrus
Amygdala
Prefrontal Cortex
Ventral Striatum
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2
Q

What type of scan shows activity dependent changes in blood flow, metabolism or bch activity?

A

PET

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3
Q

what type of scan shows detailed spatial images of the brain?

A

MRI

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4
Q

What happens to gray matter volume in the brain in depression?

A

decreased in all areas, except maybe the amygdala

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5
Q

What happens in cell counts and cell markers in depression

A

they all go down

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6
Q

t/F: there are a reduced number of synapses and glial cells in depression and reduced neuronal size

A

true

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7
Q

does blood flow increase or decrease in depression?

A

INCREASED to the mediodorsal nucleus of the thalamus, orbital and medial prefrontal cortex and to the amygdala

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8
Q

Increased metabolism in what area of the brain is associated with depression severity?

A

subgenual area of the anterior cingulate cortex

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9
Q

T/F: metabolism in the anterior cingulate cortex decreases with Rx treatment resulting in decreased depression

A

true

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10
Q

Responders to antidepressant therapy have increased metabolism in what area of the brain?

A

rostral anterior cingulate cortex

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11
Q

Reserpine inhibits what part of neurotransmission that leads to depression?

A

inhibits vesicular storage of norepi, dopa, and serotonin, results in depletion

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12
Q

Iproniazid inhibits monamine oxidase resulting in…

A

elevated mood; basis for the monoamine theory of depression

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13
Q

The monoamine theory of depression involves what two chemical systems?

A

serotonergic and noradrenergic

can involve dopamine

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14
Q

What are the two nuclei involved in the serotonergic system?

A

Rostral raphe nuclei

Caudal raphe nuclei

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15
Q

What are the two nuclei involved in the noradrenergic system?

A

lateral tegmental NA cell system

locus ceruleus

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16
Q

Antidepressant effects are likely due to adaptive changes in the CNS that happen (immediately/over time)

A

over time

17
Q

What are the long term enhancement of monoamine transmission?

A
  1. desensitization of autoreceptors which then increases monoamine release
  2. increased activity of post synaptic monoamine receptors
18
Q

Besides changes in serotonin levels, what changes do antidepressants have on synaptogenesis

A

slow increase in nerve growth factor expression (BDNF)

BDNF needed for neural plasticity, resilience, and nuerogenesis; aka changes in synaptogenesis

19
Q

What does the neurotrophic hypothesis state?

A
  1. depression is assc’d with loss of nuerotrophic support

2. antidepressant therapy increases neurogenesis and synaptic connectivity

20
Q

in which cortical area do antidepressants increase synaptic connectivity?

A

hippocampus

21
Q

What is the effect of chronic high cortisol on the hippocampus?

A

atrophy of nuerons
death of neurons with prolonged stress leads to damage of hippocampus
decrease in BDNF

22
Q

What vet tranquilizer/party drug is an NMDA glutamate receptor agonsit that can alleviate depression by stimulating synaptogenesis?

A

ketamine

23
Q

what were the effects on depression of a single dose of ketamine?

A

a single dose of ketamine delivered via intravenous infusion alleviated depressive symptoms within hours
suicide ideation was decreased
found to be effective for patients who failed to respond to two or more conventional antidepressants (refractory depression)
also effective for bipolar disorder
effects lasted for several days to a week

24
Q

Ketmaine binds to the NMDA receptor (on the terminal surface/inside the channel)

A

inside the channel

25
Q

Glutamate binds to the NMDA receptor (on the terminal surface/inside the channel)

A

on the terminal surface

26
Q

What is the proposed mechanism for ketamine increasing synaptogenesis?

A
  1. rapidly and transiently increase glutamate transmission via INHIBITION of tonically active GABA-ergic interneurons
  2. LTP-like effect due to rapid increase in BDNF levels and AMPA receptors
27
Q

What are the concerns with using ketamine for depression?

A

ketamine has poor bioavailability when taken orally
the extent to which repeated infusions will be effective is not yet known
the safety of repeated use has yet to be determined
repeated use has the potential for abuse

28
Q

Ketamine helps label depression as (blank) disorders rather than a disorder of specific neurotransmitters

A

circuit disorders

29
Q

What is deep brain stimulation FDA approved to treat?

A

OCD

30
Q

Clinical trials are looking at what non-invasive non-drug depression treatment?

A

transcranial magnetic stimulation

Block 8 Week 1 Colt (10 decks)

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