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Neuro of DA > Exam 4 > Flashcards

Exam 4 Flashcards

1
Q

corticotropin releasing factor (CRF) neurons originating in the amygdala central nucleus do what

A

project to the locus coeruleus and activate the adrenergic component of the stress response

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2
Q

anxiolytics

A

drugs to relieve anxiety, these are sedative hypnotics or CNS depressants

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3
Q

primary mechanism of action of anxiolytics

A

enhancing GABA transmission

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4
Q

longer acting BDZs are

A

useful hypnotics, muscle relaxants, and anticonvulsants

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5
Q

Buspirone

A

partial agonist at serotonin 1A receptor, does not enhance GABA action

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6
Q

what is the therapeutic index and abuse potential of SSRIs

A

high therapeutic index, low abuse potential

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7
Q

patients with anxiety disorders have abnormal

A

ANS response, higher NE released

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8
Q

why is the amygdala important to emotion processing circuits

A

receives processed sensory and cognitive information, negative emotional stimuli activate the amygdala in humans

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9
Q

anxiety disorders may be due to an imbalance between

A

emotion generating centers and higher cortical control

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10
Q

locus coeruleus NE cells are excited by

A

synaptic input from the CRF neurons in the amygdala

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11
Q

locus coeruleus NE cells are inhibited by

A

GABA, serotonin, and stimulation of a2 adrenergic somatodendritic autoreceptors

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12
Q

benzodiazepines enhance

A

inhibitory function of GABA

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13
Q

inhibitory GABA has a major role in modulating anxiety by

A

glutamatergic neurons from the PFC stimulate GABA neurons in the amygdala

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14
Q

BDZ and barbiturates bind to what to enhance function

A

GABA a receptors

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15
Q

what other modulators also enhance GABA function

A

alcohol, naturally occurring neurosteroids

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16
Q

neurosteroid levels tend to be lower in individuals with

A

general anxiety disorder and social phobia

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17
Q

baseline levels of neurosteroids are elevated in panic disorder but drop when a panic attack is induced, indicating

A

reduced GABA control of the anxiety

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18
Q

BDZs and barbituartes have binding sites on

A

GABA a receptors

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19
Q

what are barbituarates used for

A

anesthesia, seizure control, sleep induction, sedatives, alcohol withdrawl

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20
Q

side effects of barbituarates

A

induces sleep, reduced REM sleep, mental clouding, loss of judgement, slowed reflexes

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21
Q

what can high doses of barbiturates cause

A

intoxication, coma/death from respiration, dangerous with alcohol

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22
Q

problems with barbiturates

A

rapid tolerance, severe withdrawal, low safety margin

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23
Q

desirable effects of barbiturates

A

anxiety relief, loss of inhibitions, can take the edge off of other drugs

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24
Q

BDZs are highly effective for

A

anxiety reduction, don’t have side effects of barbiturates

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25
Q

BDZ choice is based on

A

speed of onset and duration of drug action

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26
Q

acetylcholine is synthesized from

A

choline and acetyl coenzyme A, catalyzed by choline acetyltransferase (chAT)

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27
Q

ACh is loaded into synaptic vesicles by

A

VAChT

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28
Q

VAChT can be blocked by

A

vesamicol

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29
Q

acetylcholinesterase (AChE) breaks down to

A

choline and acetic acid

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30
Q

drugs that block AChE prevent

A

inactivation of ACh (this is useful for disorders in which cholinergic transmission is deficient)

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31
Q

interneurons in the striatum

A

regulate dopaminergic output in the striatum

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32
Q

low dopamine levels cause transmitter imbalance and

A

hyperactivity of cholinergic neurons (Parkinson’s)

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33
Q

basal forebrain cholinergic system (BFCS)

A

neurons in several brain areas, origin of cholinergic innervation

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34
Q

different components of the BFCS have different roles in

A

cognition

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35
Q

cholinergic projections from the medial septum and diagonal band to the hippocampus and are involved in

A

declarative memories

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36
Q

projections from the nucleus basalis/substantia innominata to the prefrontal cortex are important for

A

maintaining sustained attention

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37
Q

bursts of ACh release from BFCS neurons play a key role in

A

detecting and responding to learned sensory cues (in mice)

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38
Q

cholinergic neurons in the LDTg and PPTg stimulate

A

dopamine neurons and effect drug reward and reinforcement, as well as initiation of REM sleep

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39
Q

two acetylcholine receptor subtypes

A

nicotinic and muscarinic

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40
Q

nicotinic acetylcholine receptors are

A

ionotropic, hyperpolarizing, mediate fast excitatory responses in CNS and PNS

41
Q

how to get an ACh receptor channel to open

A

all binding sites must be occupied by ACh or another agonist (such as nicotine)

42
Q

subunit composition determines

A

key features of a receptor such as affinity of binding sites, ionic selectivity, allosteric binding sites, channel opening/closing kinetics

43
Q

ionotropic receptors can be

A

open, closed, or desensitized (channel is closed and won’t open even with bound agonist; can re-sensitize spontaneously)

44
Q

depolarization block

A

resting potential of the membrane is lost and cell cannot be excited until agonist is removed and membrane repolarized

45
Q

muscarinic receptors are

A

metabotropic, operate via second messengers

46
Q

M1, M3, M5 muscarinic receptors are

A

excitatory

47
Q

M2 and M4 muscarinic receptors are

A

inhibitory

48
Q

muscarinic receptors play an important role in

A

cognitive effects of Ach, motor function, and drug reinforcement

49
Q

principal metabolite of nicotine

A

cotinine, catalyzed by cytochrome P450 2A6

50
Q

nicotine activates

A

nicotinic cholinergic receptors (nAChRs), ionotropic and produce rapid excitatory responses

51
Q

the mesolimbic dopamine pathway from the VTA to the NAcc plays a key role in

A

reinforcement

52
Q

aversive effects of nicotine

A

nausea, dizziness, sweating, headache, palpitations, stomachache, clammy hands

53
Q

a mutation in the a5 gene results in

A

less aversion to nicotine and heavier smoking

54
Q

desensitization of central nAChRs results in

A

acute tolerance

55
Q

up regulation of nAChR levels results in

A

chronic tolerance

56
Q

nicotine resource model

A

mood control and enhanced concentration are dual motivation

57
Q

deprivation reversal model

A

alleviation of irritability, stress, and poor concentration in withdrawal

58
Q

smoking during pregnancy can cause

A

stillbirth, SIDS, low birth weight

59
Q

treatment options for nicotine addiction

A

self help materials
cessation advice
individual/group counseling
medications

60
Q

nicotine replacement therapy

A

relieves withdrawal symptoms with nicotine gum/lozenges, transdermal patch, nasal spray/inhalers

61
Q

bupropion

A

a dopamine and norepinephrine reuptake inhibitor and weak nicotine receptor antagonist

62
Q

varenicline

A

a partial agonist at high affinity nicotine receptors

63
Q

cannabis plants contain over 120 compounds called

A

phytocannabinoids

64
Q

psychoactive compound in cannabis

A

THC

65
Q

mix of dried leaves and flowering tops

A

marijuana

66
Q

dried resin consisting of fine outgrowths from top of plant

A

hashish

67
Q

organic extraction from hashish

A

hash oil

68
Q

most common form of cannabis use, typically in cigarettes

A

smoking

69
Q

inhalation of cannabis vapor

A

vaping

70
Q

dissolved cannabis oils in food

A

edibles

71
Q

what does medical marijuana treat

A

glaucoma, antiemetic, anticonvulsant, analgesic, appetite enhancer

72
Q

smoked THC is easily absorbed by

A

the lungs

73
Q

oral consumption of THC leads to

A

prolonged but poor absorption, first pass metabolism

74
Q

cannabinoid effects are primarily mediated by

A

cannabinoid receptors

75
Q

slide 15

A
76
Q

psychoactive substance that causes perceptual changes, visual hallucinations, altered awareness of the mind and body, and cognitive distortions

A

psychedelic drug

77
Q

in peyote cactus, top is cut off and dried, chewed raw or cooked

A

mescaline

78
Q

alkaloid from several mushroom species, dried and eaten raw or made into tea

A

psilocybin

79
Q

found in plants indigenous to south america, smoked or snorted, produce a brief high

A

DMT and bufotenine

80
Q

synthetic and based on fungal alkaloids

A

LSD

81
Q

drug induced psycholysis

A

psycholytic therapy

82
Q

patient was given high dose of LSD in hopes of gaining insight into problems

A

psychedelic therapy

83
Q

appeared in 2010, synthetic compound

A

NBOMes

84
Q

trip state of intoxication phases

A

onset, plateau, peak, comedown

85
Q

crossing over of sensations

A

synesthesia

86
Q

five dimensions of altered states of consciousness

A

oceanic boundlessness, ego-disintegration anxiety, visionary restructuralization, reduced vigilance, auditory alterations

87
Q

serotonin like drugs

A

LSD, psilocybin, psilocin, DMT, synthetic tryptamines

88
Q

catecholamine like drugs

A

mescaline and NBOMes

89
Q

PCP and ketamine are

A

dissociative anesthetics

90
Q

non competitive antagonists at the ionotropic NMDA receptor (bind to a site within receptor’s channel blocking ion flow)

A

PCP and ketamine

91
Q

remains trapped in the channel even after the agonist (glut) dissociates from binding site and channel closes

A

drug molecule

92
Q

the NMDA receptor blockade on cortical GABAergic interneurons increases

A

cortical glutamate release

93
Q

what drugs activate the midbrain dopamine cell firing and stimulate dopamine release in the dorsal striatum, NAcc, PFC

A

PCP and ketamine

94
Q

increases in drug liking and desire for more drug is

A

dose dependent

95
Q

other non competitive NMDA receptor antagonist

A

dextromethorphan (OTC cold medication)

96
Q

biopsychosocial model of addiction

A

includes full range of pharmacological, biological, and psychological factors that influence addiction risk

97
Q

incentive sensitization theory of addiction

A

distinction between liking vs wanting a reward

98
Q

negative emotional state evoked by drug withdrawal

A

hyperkatifeia

Neuro of DA (3 decks)

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