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PSYT 500 - PRE-MIDTERM > Neurochemistry > Flashcards

Neurochemistry Flashcards

1
Q

how did COVID affect mental disorder prevalence?

A

MDD and anxiety increased a lot in young people, especially females

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2
Q

how did we used to think about mental disorders?

A

Freudian psychoanalytic theories

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3
Q

what suggested the biological basis of mental disorders in the 50s?

A

serendipitous discovery of drugs like chlorpromazine and lithium

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4
Q

chlorpromazine

A

mild tranquilizer; typical antipsychotic

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5
Q

lithium

A

anti-mania drug

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6
Q

DSM definition of mental disorder

A

clinically significant behavioural or psychological syndrome or pattern that occurs in an individual and that is associated with present distress and/or disability

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7
Q

what is the DSM?

A

a categorical classification that divides mental disorders into types based on criteria sets with defining features

not necessarily completely discrete entities

atheoretical regarding causes of mental disorders—classifies by symptoms, not cause

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8
Q

what is the point of the DSM?

A

trying to ‘standardize’ diagnoses a bit

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9
Q

critiques of the DSM

A
  • genetic studies do not support the discreet classification system
  • no biological basis for diagnoses
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10
Q

Research Domain Criteria Project (RDoC)

A

a new initiative that aims to guide the classification of mental disorders by underlying biology and quantifiable things

looks at genetics, imaging, cog sci, and other factors

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11
Q

constructs of RDoC

A

constructs = the parameter you’re measuring

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12
Q

what do you do with the RDoC constructs?

A

group them into domains of functioning based on vibes

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13
Q

domains of RDoC

A

negative valence systems, positive valence systems, cognitive systems, systems for social processes, and arousal/regulatory systems

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14
Q

valence

A

the value associated with a stimulus as expressed on a continuum from pleasant to unpleasant or from attractive to aversive.

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15
Q

how common is glutamate?

A

90% of neurons use glutamate; 80-90% of synapses are glutamatergice

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16
Q

how can glutamate signaling be precise if it’s so common?

A

its release is quickly terminated and transporters reuptake it so there’s no over-excitation

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17
Q

two flavours of GluR

A

iGluR; mGluR

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18
Q

why are NMDARs a sexy drug target?

A

NMDAR are involved in working memory and excitatory transmission, so good anaesthetic or learning drug!

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19
Q

why are NMDARs not a good drug target?

A

NMDAR cause psychosis when antagonized like you’d want for an anaesthetic (PCP, ketamine)

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20
Q

pros of ketamine as an antidepressant

A

fast-acting

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21
Q

extrasynaptic NMDARs

A

linked to cell death

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22
Q

synaptic NDMARs

A

linked to cell survival

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23
Q

norepinephrine

A

arousal and alertness, regulates memory formation by emotion

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24
Q

where are norepinephrine neurons?

A

locus coeruleus

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25
Q

locus coeruleus

A

area of the brainstem that contains norepinephrine; involved in memory formation

has all the NE cell bodies. project where they’re needed

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26
Q

norepinephrine synthesis

A

Tyrosine -> DOPA -> Dopamine -> Norepinephrine

27
Q

what does dopamine B hydrozylase (DBH) do?

A

final step of dopamine -> NE

28
Q

what do mutations in DBH do?

A

lead to lack of arousal because no NE

  • non-fatal
  • patients do fine in school/life, but not sporty and faint a lot
29
Q

experiment linking NE and memory

A

two groups of subjects read two different plots designed to elicit different reactions

the groups were asked to remember details later. You’d expect the arousal group to recall more accurate, vivid details/have a better remembering score compared to the neutral version

but when group with arousal plot treated with NE blocker (propranolol) they don’t remember more compared to the neutral plot, so NE is def involved in the emotional content of remembering an event

30
Q

amygdala

A

A limbic system structure involved in memory and emotion, particularly fear and aggression.

31
Q

how does the amygdala affect the LC?

A

activates the locus coeruleus with CRH

32
Q

How does the locus coeruleus affect memory formation?

A

fibers from LC release NE to the basolateral amygdala and hippocampus, activating neurons in regions related to fear AND memory = stronger memories when you’re scared

33
Q

how does cortisol affect memory?

A

reduces the activity of the basolateral amygdala and central amygdala AND the dentate gyrus and CA1 neurons in the hippocampus = less memory encoding during stress

34
Q

dentate gyrus

A

a layer of neurons in the hippocampus that receives input from the entorhinal cortex

35
Q

catecholamines

A

dopamine, norepinephrine, epinephrine

hormones secreted by the adrenal medulla that affect the sympathetic nervous system in stress response

36
Q

what’s the point of stress?

A
  • heightened excitability or arousal
  • induce aversiveness
  • lack of controllability
37
Q

glucocorticoids

A

Synthesized and released by the adrenal cortex, glucocorticoids raise blood glucose levels while decreasing protein synthesis to get you ready for the ‘fight or flight’

38
Q

mineralcorticoid receptors

A

activated at basal levels. does homeostasis

39
Q

glucocorticoid receptors

A

activated at stress levels of cortisol. do stress response

40
Q

HPA axis

A

the hypothalamus, pituitary gland, and adrenal cortex

Interaction between the nervous and endocrine systems to produce the body’s response to stress. Elevated levels of one of these hormones may lead to depression

41
Q

allostatic load

A

the long-term negative impact of the stress response on the body

42
Q

allostasis

A

process by which the body achieves stability through physiological change

LONG TERM modification of body over the long term

43
Q

allostasis/adaptation vs maladaptation

A

if you have some water to put out the fire, nice! if you have too much water, now you have damage caused by water

44
Q

dopamine

A

reward! motivation! happy! addiction!

45
Q

mesolimbocortical pathway

A

a set of dopaminergic axons arising in the midbrain and innervating the limbic system and cortex. involved in bipolar disorder

46
Q

dopamine synthesis pathway

A

tyrosine –Tyrosine Hydroxylase–> L-DOPA –Dopa Decarboxylase–> Dopamine

47
Q

cocaine MOA

A

Blocks dopamine and NE uptake in the reward receptors in the brain (floods dopamine and NE in the synapse)

48
Q

amphetamine MOA

A

a substrate that is more preferred than dopamine = dopamine agonist

forces active release of DA from terminal

49
Q

5HT endogenous function

A

cardio, respiratory, sleep, aggression, sexual behaviour, nutrient intake, mood, motor output, nociception/analgesia, neuroendocrine fxn

50
Q

SERT blockers do what?

A

antidepressant

51
Q

raphe nucleus

A

A group of serotonin-containing neurons extending from the raphe nuclei, located in the pons and medulla throughout the limbic system and forebrain

52
Q

subdivisions of raphe nucelus

A
  • rostral -> dorsal and median
  • caudal
53
Q

rostral raphe projections

A

brain—contain 85% of serotonin neurons in the brain!

54
Q

caudal raphe projections

A

spinal cord

55
Q

dorsal raphe neurons

A

fine and rarely make synaptic contacts

56
Q

medial raphe neurons

A

coarser axons and synaptic specialization

57
Q

5HT synthesis pathway

A

l-tryptophan -> 5-HTP -> 5-HT

58
Q

SERT gene

A

SCL6A4

59
Q

SERT gene polymorphisms

A

long GC-rich promoter w/ 16 repeats or short 14 repeats

60
Q

long vs. short SERT polymorphism effects

A

short form increases risk of depression

61
Q

what happens with chronic exposure to SSRIs?

A

decreases 5-HT uptake by internalization and degradation of SERT (chemical dependence)

62
Q

non-vesicular release of 5HT caused by?

A

ecstasy

63
Q

non-vesicular release of 5HT mechanism

A

ecstasy blocks VMAT, so 5HT builds up in cytoplasm, which reverses the presynaptic transporter, which then pumps out 5HT without vesicles

64
Q

VMAT

A

vesicular monoamine transporter

PSYT 500 - PRE-MIDTERM (3 decks)

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