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neuro of da > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

serotonin is synthesized from what

A

tryptophan

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2
Q

two steps to serotonin synthesis

A

catalyzed by TPH and AADC

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3
Q

TPH2

A

in serotonergic neurons

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4
Q

how is serotonin synthesis regulated

A

enzymatic activity and precursor activity

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5
Q

why does tryptophan compete with amino acids

A

to cross the blood brain barrier and increase serotonin

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6
Q

what diet increases ratio of tryptophan

A

low protein high carbohydrate

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7
Q

what does elevating tryptophan do

A

enhance cognitive functions (memory, attention), elevate mood, improve sleep

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8
Q

tryptophan loading

A

administration of pure tryptophan

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9
Q

if you inhibit TPH you get

A

less serotonin

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10
Q

reducing serotonin via ATD method does what

A

impairs memory consolidation of verbal information but has no influence on working memory and attention

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11
Q

serotonin is transported into synaptic vesicles by

A

VMAT2

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12
Q

reserpine does what

A

depletes serotonin (broken down when not in vesicles)

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13
Q

terminal autoreceptors do what to serotonin

A

directly inhibit release

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14
Q

somato-dendritic autoreceptros do what to serotonin

A

inhibit release by slowing rate of nerve firing

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15
Q

what reuptakes serotonin

A

SERT

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16
Q

antidepressant drugs

A

SSRI’s

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17
Q

how do SSRIs work

A

by blocking the serotonin transporter

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18
Q

where are serotonergic neurons found

A

along the midline of the brainstem (raphe nuclei)

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19
Q

what are the roles of dorsal raphe nucleus (DRN) and median raphe nucleus (MRN)

A

give rise to most of the serotonergic fibers in forebrain

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20
Q

when awake, how do serotonin cells fire

A

a regular rate (tonic firing)

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21
Q

how do serotonin cells fire when in slow wave sleep

A

irregularly

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22
Q

slow tonic firing of DRN neurons promotes what

A

non REM sleep

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23
Q

burst firing of DRN neurons promotes what

A

wakefulness

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24
Q

where is serotonin 1a receptor concentrated

A

in hippocampus, septal area, and DRN

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25
Q

what does the serotonin 1A receptor do

A

inhibit adenylyl cyclase to decrease cAMP, increase opening of K+ channels and membrane hyperpolarization

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26
Q

what kind of receptor is serotonin 1A

A

autoreceptor and postsynaptic

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27
Q

where are serotonin 2A receptors located

A

cortex

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28
Q

what do serotonin 2a receptors do

A

increase Ca2+ levels in postsynaptic cell and activate protein kinase C

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29
Q

what kind of receptor is serotonin receptor 2A

A

activating

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30
Q

most serotonergic neurons in the CNS are located

A

raphe nuclei

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31
Q

serotonin has a key role in regulation of

A

anxiety through postsynaptic serotonin 1A receptors

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32
Q

serotonin deficiency hypothesis

A

low CNS serotonergic activity is associated with hyper aggressiveness

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33
Q

what is a behavior/function influenced by serotonin

A

anxiety, appetite, and sleep

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34
Q

what does MDMA do

A

stimulates release of serotonin from nerve terminals and inhibits reuptake

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35
Q

effects of MDMA

A

heightened arousal, euphoria, enhanced perceptual awareness, prosocial effects

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36
Q

high MDMA doses result in

A

serotonin depletion (in animals)

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37
Q

designer drugs

A

synthetic cathinone and amphetamine variants

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38
Q

synthetic cathinones

A

are substrates for dopamine, norepinphrine, and serotonin transporters, and cause acute release of dopamine, serotonin, and norepinephrine

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39
Q

what kind of drugs are opioids

A

narcotic analgesics (reduce pain without producing uncosciousness)

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40
Q

psychoactive ingredients in opiates

A

morphine and codeine

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41
Q

partial agonists

A

less analgesic effect, reduced risk of dependence

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42
Q

antagonist

A

can prevent or reverse effects of opioids (treatment for overdose)

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43
Q

which reaches the brain faster: heroin or morphine

A

heroin

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44
Q

adverse affects of opoids

A

restlessness, anxiety, nausea/vomiting

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45
Q

higher doses of opiods

A

abnormal state of elation or euphoria

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46
Q

low to moderate dose of opioid

A

pain relief, constricted pupils, drowsiness, inability to concentrate, dreamy sleep

47
Q

respiratory failure is the ultimate cause of death in overdose because

A

morphine acts on the brainstem’s respiratory center

48
Q

how can naloxone’s blocking effects be overcome

A

by increasing concentrations of morphine, showing competition for the receptor

49
Q

types of opioid receptors

A

mu, delta, and kappa

50
Q

mu receptors

A

have a high affinity for morphine, wide distribution in brain and spinal cord

51
Q

delta receptors

A

found in forebrain, modulate olfaction, motor integration, reinforcement, and cognitive function

52
Q

kappa receptors

A

found in striatum and amygdala, hypothalamus and pituitary, participate in regulation of pain perception, gut motility, and dysphoria

53
Q

all opioid receptors are coupled to

A

G proteins (metabotropic, all inhibitory)

54
Q

postsynaptic inhibition

A

opens potassium channels, hyperpolarization

55
Q

axoaxonic inhibition

A

closes calcium channels, decreases amount of transmitter released

56
Q

presynaptic autoreceptors

A

reduce release of a co-localized transmitter

57
Q

mu and delta receptor join to form

A

a heterodimer

58
Q

opioid ligands are

A

peptides

59
Q

mu receptor binds to

A

endomorphins and endorphins

60
Q

delta receptor binds to

A

enkephalin

61
Q

kappa receptor binds to

A

dynorphins

62
Q

first (early) pain

A

immediate, sensory component, goes from spinal cord to thalamus

63
Q

second (late) pain

A

emotional component, goes to anterior cingulate cortex

64
Q

opioids reduce transmission of pain signals at the spinal cord in two ways

A

inhibitory spinal interneurons: release endorphins that inhibit activation of spinal projection neurons
descending modulatory pathways: inhibit projection neuron or excitatory interneuron, or excite inhibitory opioid neuron

65
Q

opioid drugs inhibit

A

inhibitory GABA cells, increasing mesolimbic cell firing and dopamine release in NAcc

66
Q

cross tolerance

A

related drugs also show reduced effectiveness

67
Q

physical dependence

A

lack of drug causes withdrawal

68
Q

cross dependence

A

administering any other opioid drug will stop or reduce withdrawal

69
Q

acute effects of opioids are the opposite of

A

withdrawal symptoms

70
Q

methadone

A

reduces symptoms to a comfortable level, reduces euphoric effect of heroin

71
Q

clonidine

A

acts on noradrenergic autoreceptors to reduce norepinephrine activity in locus coeruleus

72
Q

buprenorphine

A

opioid partial agonist used in the same way as methadone

73
Q

medication assisted treatment

A

a combination of detoxification, pharmacological support, and group/individual counseling

74
Q

glutamate

A

ionized form of glutamic acid formed from glutamine (an excitatory amino acid neurotransmitter)

75
Q

vesicular glutamate

A

transporters move glutamate into synaptic vesicles: VGLUT1, 2, and 3

76
Q

glutamate uptake

A

5 different excitatory amino acid transporters (EAATs)

77
Q

astrocytes

A

express EAAT2 and may account for about 90% of total glutamate uptake

78
Q

astrocyte transporters

A

convert the glutamate uptaken to glutamine using glutamine synthetase

79
Q

ionotropic glutamate receptors

A

depolarize the membrane of the postsynaptic cell (excitatory)

80
Q

AMPA receptor

A

fast excitatory responses to glutamate

81
Q

Kainate receptor

A

selective agonist kainic acid

82
Q

NMDA receptor

A

allows both Na and Ca to pass, agonist NMDA

83
Q

unique characteristics of NMDA receptors

A

simultaneous binding of glutamate and a co-agonist

binding site for Mg in the ion channel

channel only opens if both co-agonist binding and depolarization of cell membrane occur

84
Q

metabotropic glutamate receptors

A

group 1: postsynaptic, activate second messenger system, excitatory

group 2 and 3: presynaptic, reduce transmitter release, inhibit cAMP formation, autoreceptors

85
Q

long term potentiation

A

release of glutamate coupled with strong activation of NMDA receptors can lead to strengthening of that synapse

86
Q

excitotoxicity hypothesis

A

excessive exposure to glutamate causes prolonged depolarization of receptive neurons, leading to damage or death

87
Q

GABA

A

major inhibitory amino acid transporter

88
Q

GABA is synthesized from

A

glutamic acid decarboxylase (GAD)

89
Q

moves GABA into vesicles

A

VGAT

90
Q

GABA is metabolized to succinate by

A

GABA-T

91
Q

GABA a receptor

A

ionotropic, causes hyperpolarization and inhibition of postsynaptic cell, consists of 5 subunits

92
Q

GABA a receptors are sensitive to

A

CNS depressant drugs

93
Q

GABA b receptor

A

metabotropic, postsynaptic, inhibits neuronal firing and adenylyl cyclase

94
Q

Presynaptic GABA b receptors inhibit

A

transmitter release and adenylyl cyclase

95
Q

diverse group of compounds that depress the CNS and behavior

A

alcohol, barbiturates, non-barbiturate hypnotics, anxiolytics

96
Q

the calming of mental excitement or abatement of physiological function

A

sedation

97
Q

to produce sleep

A

hypnosis

98
Q

behavioral effects of alcohol are described through

A

blood alcohol concentration (BAC)

99
Q

alcohol is oxidized by

A

alcohol dehydrogenase and aldehyde dehydrogenase (ALDH)

100
Q

when alcohol is consumed on a regular basis, these liver enzymes increase in number, increasing the rate of metabolism of alcohol/other drugs

A

induction

101
Q

in a single exposure, effects are greater while blood level is rising and smaller while blood level is falling

A

acute tolerance

102
Q

increase in P450 liver microsomal enzymes that metabolize alcohol

A

metabolic tolerance

103
Q

neurons adapt to continued presence of alcohol by making compensatory changes in cell function

A

pharmacodynamic tolerance

104
Q

practicing behaviors while under the influence of alcohol allows adjustment and compensation

A

behavioral tolerance

105
Q

intensity and duration of withdrawal is dependent on amount and duration of drug taking

A

physical dependence

106
Q

permanent damage to thalamic nuclei and brain regions involved in memory subsequent to vitamin B1 deficiency

A

korsakoff syndrome

107
Q

symptoms of fetal alcohol syndrome

A

intellectual disability, developmental delays, low birthweight, neurological problems, head/facial malformation

108
Q

why are animal models vital for alcohol research

A

kept in controlled environment, eliminates poor nutrition, psychiatric disorders, other drug use, genetic engineering can be used

109
Q

cell membrane lipids become more fluid, changes relationship with membrane proteins

A

nonspecific action

110
Q

influences ligand gated channels and alters second messenger systems

A

specific actions

111
Q

acute alcohol inhibits

A

glutamate transmission and glutamate release

112
Q

acute alcohol increases

A

GABA effects at GABA a receptor

113
Q
A

neuro of da (3 decks)

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