Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

Neurobiology of Depression- Craviso Flashcards

1
Q

What areas of the brain are involved with regulation of mood and emotion expression, reward processing, attention, motivation, stress response, and neuro-vegetative function?

A
  • hypothalamus
  • hippocampus
  • cingulate gyrus
  • amygdala
  • prefrontal cortex
  • ventral striatum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What makes up the limbic system?

A

Hippocampus
Hypothalamus
Amygdala

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Is the a diagnostic blood or brain test for depression?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are some neuro-imaging techniques to check for depression (not diagnosis it)?

A

PET-check brain blood flow, tissue metabolis, biochemical activity
MRI- spatial images of brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

In depressed patients what happend to their gray matter?

In depressed patients what happened to their cell counts and cell markers?

A

decreased in hippocampus, cingulate gyrus, amygdala, prefrontal cortex, ventral striatum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

In addition to decreased gray matter volume and cell counts, what else do depressed patients have decreased amounts of?

A

-reduced number of synapses and gial cells, reduced neuronal size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

In depressed peope their is an increase in (Blank) especially in the orbital and medial prefrontal cortex and the amygdala.

A

blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where do you see an abnormality in the brain of depressed patients and correlates positively with depression severity?

A

anterior cingulate cortex subgenual area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In major depression and even in response to scripts that induce transient sadness you will see increased activity in the (BlanK) but activity will return to normal with successful pharm treatment

A

ACC (anterior cingulate cortex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

In depressed patients, did they have elevated or depressed metabolism in the rostral anterior cingulate cortex?
Is it better or worse to have more metabolic activity?

A

elevated

better-> indicates better response to treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What did reserpine, a blood pressure med, also do?

A

induce depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What did iproniazid, a drug used to treat TB, also do?

A

induce signif mood-elevation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does reserpine work?

A

inhibits vesicular storage of biogenic amines (NE, dopamine serotonin) resuting in their metabolism by monoamine oxidase.
I.e got rid of NE, dopamine and 5HT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the major consequence of reserpine?

A

depletes neuronal stores of biogenic amines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What does iproniazid do?

A

inhibits intraneuronal monoamine oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the consequence of iproniazid?

A

increase levels of biogenic amines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the monoamine hypothesis of depression?

A

depression viewe as a deficit of biogenic monoamines (particularly norepinephrine and serotonin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where does the serotonergic system begin and where does it project to?

A

raphe nuclei-> project to the cortices, cerebellar cortex, limbic system, spinal cord, nucleus accumbens, neocortex, cingulate gyrus, deep cerebellar nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where does the noradrenergic system begin and where does it project to?

A

locus ceruleus and lateral tegmental NA cell system-> project to thalamus, cingulat gyrus, limbic system, neocortex, cerebellar cotex, spinal cord

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Is the monoamine hypothesis of depression accurate?

A

sort of, it is too simplistic … a single drug cannot restore balance among all the interacting neuronal networks involved… this is proved by the delayed effects of antidepressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

About (blank) percent of patients respond in the short-term to antidepressants; total remission of systoms around (blank)

A

60-70%

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

So why do antidepressants work if they monoamine hypothesis isnt accurate?

A

because the antidepressants eventally change the structure of the CNS make new synapses and such which is what treats the patient… i,e its what the monoamines can do, not the lack of the monoamines themselves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Most clinicaly used antidepressant drugs rapidly increase (Blank) levels whereas therapeutic effects are delayed by (blanK)

A

biogenic amine

several weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are antidepressant effects likely due to?

A

adaptive changes in the CNS that take time to develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the adaptive changes identified with antidepressants that increase biogenic monoamines?

A

long-term enhancement of monoamine neurotransmission

26
Q

What is the long-term enhancement of monoamine transmission due to?

A
  • desensitization of autoreceptors on monamine nerve terminals (reduces negative feedback and therefore increases release of monoamines)
  • increased activity of certain post-synaptic monoamine receptors
27
Q

What is the neurotrophic hypothesis of depression?

A

depression is associated w/ loss of neurotrophic support

28
Q

How do you treat depression if you believe in the neurotrophic hypothesis?

A

antidepressant that increase neurogenesis and synaptic connectivity in cortical areas such as the hippocampus (neural plasticity/ changes in neural network connectivity)

29
Q

What can antidepressants do other than increase biogenic amine levels?

A

cause an increase in nerve growth factor expression (i.e BDNF)-> critical in regulation of neural plasticity, resilience and neurogenesis

30
Q

What does increasing BDNF result in?

A

long term adaptive changes that result in synaptogenesis

31
Q

T or F
Depression and stress are interrelated
Which hypothesis does this support?

A

T

neurotrophic hypothesis

32
Q

How is stress and depression related?

A

stress results in increased cortisol levels which results in atrophy of neurons in the hippocampus

33
Q

Chronic stress decreases (blank)

A

BDNF

34
Q

In a depressed state, you will have increased glucocorticoids that will inhibit (blank) and result in decrease synaptogenesis and result in neuron atrophy

A

BDNF

35
Q

In the treated state of depression you have increase in (Blank) inducing synaptogenesis.

A

BDNF

36
Q

What does LTP do?

A

increases sensitivity of post-synaptic neurons to glutamate-> eventually results in synaptogenesis

37
Q

How can you speed of synaptogenesis?

A

with electro therapy

38
Q

GABA B presynpatically gets bound by Gaba and (blank) calcium influx which results in decreased release of GABA

A

decreases

39
Q

What do the GABA receptors do postsynaptically

A

Postsynaptically GABA B receptors will bind GABA and let potassium out or reduce calcium influx and hyperpolarize membrane along with GABA A which will give Cl- ions to hyperpolarize membrane.

40
Q

What drug can super fast speed up synaptogenesis?

A

ketamine

41
Q

How does ketamine work?

A

in mysterious ways, it is an NMDA glutamate receptor antagonist that somehow increases glutamate neurotransmission

42
Q

A single dose of ketmine delivered via IV infusion alleviated depressive symptoms within (Blank)

A

hours

43
Q

Ketamine reduced (blank) ideation

A

suicidal

44
Q

Ketamine was found to be effective for patients who failed to respond to (blank) or more conventional antidepressants (refractory depression)

A

2

45
Q

Ketamine is effective for (blank) disorder

A

bipolar

46
Q

How long do the effects of ketamine last?

A

days to weeks

47
Q

WHere does ketamine bind in the NMDA receptor?

A

inside and works as an antagonist

48
Q

What are the clinical manifestations of ketamine use?

A

dissociative symptoms and anesthesia

49
Q

SOOO how ketamine promote synaptogenesis if it is a NMDA inhibitor?

A

dont really know, proposed to rapidly and transiently increase glutamate neurotransmission, possibly by inhibition of tonically active GABA-ergic interneurons

50
Q

Ketamine has an LTP-like effect due to a rapid increase in (blank) levels and (blank) receptors

A

BDNF

AMPA

51
Q

Ketamine rapidly causes (blank)

A

synaptogenesis

52
Q

How should you give ketamine and why?

A

IV cuz it has poor bioavailability when taken orally.

53
Q

Ketamine needs to be researched more and does have some potential for abuse but its positive effects on (Blank) has had a meaningful impact on the future development of novel therapeutics for depression

A

depression

54
Q

Mental disorders are (blank) disorders- so less specific neurotransmitters, more about synaptogenesis and neuroplasticity.

A

circuit

55
Q

What is the non-pharmacological way to treat depression and induce synaptogenesis?

A

Deep brain stimulation

56
Q

What is deep brain stimulation?

A

electric stimulation “quiets” the overactive region-alters excitability by affecting neural networks (synaptogenesis/neural plasticity)

57
Q

What is ECT?

A

intentionally triggers a brief seizure

58
Q

Why does DBS only work for a small amount of time?

A

because as the natural progression of the disease continues you lose neurons to perform DBS on

59
Q

DBS is approved by the FDA to treat severe (blank)

A

OCD

60
Q

What is in clinical trials to assess other ways of stimulation to treat depression?

A

transcranial magnetic stimulation (TMS) -non-invasive

Block 8 Week 1 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions