Neuropharm Final Flashcards

1
Q

what is pharmacology?

A

the scientific study of the actions of drugs and their effects on a living organism

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2
Q

define pharacokinetics

A

how substances are distributed through the body

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3
Q

define pharmacodynamics

A

interactions of the substance with a receptor

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4
Q

define neuropharmacology

A

drug-induced changes in nervous system functions

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5
Q

define psychopharmacology

A

drug-induced changes in mood, thinking, and behavior

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6
Q

define neuropsychopharmacology

A

drug-induced changes in the nervous system that influence behavior

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7
Q

what is a drug action?

A

a specific molecular change

drug binds to its target (receptor)

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8
Q

what is a drug effect?

A

a more widespread/systemic change

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9
Q

what are therapeutic effects?

A

desirable drug effects

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10
Q

what are side effects?

A

undesirable drug effects?

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11
Q

what are specific drug effects?

A

results from interactions btwn a drug and its target

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12
Q

what are nonspecific drug effects?

A

include mood, expectations, perceptions, attitudes

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13
Q

what is pharmacokinetics?

A

mechanisms involved in delivering a drug to its target, where it can have pharmacological effect

-administration
-absorption
-distribution
-elimination
—–metabolism and excretion

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14
Q

what is bioavailability?

A

the amount of drug in the blood that is free to act on a specific target

–depends on absorption, distribution, elimination

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15
Q

what are pharmacodynamics?

A

interactions btwn the drug and its target; mechanisms of drug action

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16
Q

describe lipid-receptor interaction

A

–dynamic and reversible
–in a constant state of binding and breaking away
–follows the law of mass action

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17
Q

how do you determine non-specific binding?

A

a very high concentration of unlabeled ligand is added, outcompeting the hot radioligand for specific binding sites

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18
Q

what is an agonist?

A

drug that mimics the effect of the endogenous transmitter

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19
Q

what is a partial agonist?

A

drug that cannot produce the full agonist response

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20
Q

what is an antagonist?

A

drug that block the effect of the endogenous transmitter

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21
Q

what is receptor affinity?

A

how tightly the receptor holds onto the drug
—lock and key mechanism

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22
Q

what is drug potency?

A

the amount of drug necessary to produce a desired level of effect

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23
Q

what is drug efficacy?

A

the maximum response produced by a drug

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24
Q

what is a competitive antagonist?

A

“compete” w the agonist for binding to the agonist binding site
***high affinity for the agonist binding site, but no efficacy

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25
Q

what is a non-competitive antagonist?

A

bind to a site different from the agonist binding site
***negative allosteric modulation

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26
Q

a competitive antagonist shifts the dose-response curve to the _____?

A

right

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27
Q

what is another name for the myelencephalon?

A

medulla

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28
Q

what is another name for the mesencephalon?

A

midbrain

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29
Q

what brain structures make up the metencephalon?

A

cerebellum and pons

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30
Q

what brain structures make up the diencephalon?

A

thalamus and hypothalamus

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31
Q

what brain structures make up the telencephalon?

A

neocortex, basal ganglia, limbic system

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32
Q

describe ligand-gated ion channels

A

–ionotropic
–fast transmission
–no intermediate chemical steps
–directly changes membrane permeability

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33
Q

describe G protein-coupled receptor

A

–metabotropic
–slow activation
–long-lasting effects
–alters intracellular biochemistry

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34
Q

terminal autoreceptors are _____-modulating

A

release

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35
Q

somatodendritic autoreceptors are _______-modulating

A

activity

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36
Q

the morris water maze is a test of ________

A

spatial learning

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37
Q

the open field test is a measure of _______

A

motor activity

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38
Q

the delayed-response tests is a measure of ______

A

working memory

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39
Q

the light-dark box measures ________

A

unconditioned anxiety

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40
Q

the elevated plus-maze measures ________

A

unconditioned anxiety

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41
Q

the forced swim test measures _______

A

behavioral dispair

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42
Q

the sucrose preference test is a measure of _______

A

anhedonia, the inability to derive pleasure from normally pleasurable events

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43
Q

drug self-administration measures _______

A

reinforcement value of substances

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44
Q

define breaking point

A

point at which effort required exceeds reinforcing value– the higher the breaking point, the higher the abuse potential

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45
Q

drug discrimination studies measure _____

A

how an animal experiences a drug

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46
Q

what are the ionotropic receptors for ACh?

A

nicotine
curare

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47
Q

what are the metabotropic receptors for ACh?

A

muscarine
atropine

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48
Q

what is the rate-limiting step of ACh synthesis?

A

choline uptake into nerve terminal

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49
Q

what does vesamicol do?

A

blocks VAChT
reduces amount of ACh released when the neurons fire

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50
Q

what does black widow spider venom do to ACh release?

A

massive release of ACh in the PNS
–muscle pain, tremors, nausea, vomiting, salivation, copious sweating

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51
Q

what does botulinum toxin do to ACh release?

A

inhibits ACh release

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52
Q

which drug is used to treat glaucoma?

A

physostigmine

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53
Q

which drug is used to treat myasthenia gravis?

A

neostigmine and pyridostigmine

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54
Q

does physostigmine cross the BBB?

A

yes!

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55
Q

do neostigmine and pyridostigmine cross the BBB?

A

nope!

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56
Q

what are the reversible AChE inhibitors?

A

donepezil and rivastigmine

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57
Q

what are organophosphates?

A

irreversible AChE inhibitors
**insecticides
**
nerve agents

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58
Q

describe the nAChR

A

5 subunits are arranged around a central pore
-each subunit has 4 TMDs

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59
Q

homomeric nACh receptor is permeable to which ion?

A

calcium!

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60
Q

what is an agonist for nAChR?

A

nicotine

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61
Q

what is an antagonist for nAChR?

A

curare

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62
Q

describe the mAChR

A

M1-M5

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63
Q

what is an agonist for mAChR?

A

muscarine

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64
Q

what is an antagonist for mAChR?

A

atropine
scopolamine

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65
Q

what does ACh do in cognition?

A

memory consolidation
sensory attention
behavioral arousal

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66
Q

deficits in ACh signaling are involved in _______

A

dementia

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67
Q

mACh receptor antagonists are ______ and impair performance on ______

A

amnestic
learning tasks

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68
Q

ACh synthesis

A

choline + acetyl CoA

—-choline acetyltransferase

acetylcholine

—-acetylcholinesterase

choline + acetic acid

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69
Q

what is the most abundant excitatory neurotransmitter in the brain?

A

glutamate!

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70
Q

glutamate synthesis

A

glutamine

—-glutaminase

glutamate

—-glutamine synthetase

glutamine

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71
Q

what is the most abundant inhibitory neurotransmitter in the brain?

A

GABA

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72
Q

ionotropic glutamate receptors

A

NMDA
AMPA
KA

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73
Q

metabotropic glutamate receptors

A

group 1 (1 and 5)
group 2 (2 and 3)
group 3 (4, 6, and 7)

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74
Q

which iGlu receptors are permeable to ca2+?

A

NMDA
AMPA lacking GlueA2

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75
Q

properties of NMDA receptors

A

ligand-gated ion channels, requiring co-agonists glu and gly

voltage gated
–removal of Mg2+ block

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76
Q

GABA a ionotropic receptors

A

permeable to Cl- leading to hyperpolarization

two alpha, two beta, and one gamma subunit

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77
Q

what is a GABA binding site agonist

A

muscimol

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78
Q

what is a GABA binding site competitive antagonist

A

bicucculine

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79
Q

GABA b receptors are ______

A

metabotropic

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80
Q

what do postsynaptic GABAb receptors do

A

open k+ ion channels
inhibition of AC/ decrease cAMP

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81
Q

what do presynaptic GABAb receptors do

A

autoreceptors, heteroceptors

inhibition of Ca2+ channels
inhibition of AC/ decrease cAMP

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82
Q

what are positive allosteric modulators for GABA a

A

benzodiazepines
barbiturates
neurosteroids, EtOH, Anesthetics

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83
Q

what are negative allosteric modulators of GABAa

A

pictrotoxin

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84
Q

behavioral effects due to a-1

A

sedation (Ambien)

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85
Q

behavioral effects due to a-2/3

A

anxiolytic (Xanax)

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86
Q

behavioral effects of a-5

A

amnestic

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87
Q

how do you obtain tyrosine?

A

In diet

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88
Q

catecholamines synthesis

A

tyrosine –(TH/Fe2+, O2, BH4)—> L-DOPA –(AADC/vitamin b6)–> dopamine –(DBH/cu2+, o2, ascorbic acid)–> norepinephrine –(SAM)–> epinephrine

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89
Q

what is the rate-limiting step in catecholamine synthesis?

A

TH

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90
Q

AMPT

A

TH inhibitor

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91
Q

Reserpine

A

irreversible VMAT inhibitor

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92
Q

tetrabenazine, deutetrabenazine, valbenazine

A

reversible VMAT inhibitor

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93
Q

6-OHDA and MPTP

A

DA neurotoxins

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94
Q

amphetamine

A

catecholamine releaser and reuptake blocker

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95
Q

cocaine

A

catecholamine reuptake blocker

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96
Q

what is a noradrenergic alpha2 autoreceptor agonist

A

clonidine

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97
Q

what is a noradrenergic alpha 2 autoreceptor antagonist

A

yohimbine

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98
Q

where is the nigro-striatal pathway located and what is it in control of?

A

substantia nigra

activation, motivation, cognition

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99
Q

where is the mesolimbic system located and what is it in charge of?

A

VTA

behavioral arousal, reward learning

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100
Q

where is the mesocortical system located and what is it in charge of?

A

VTA

attention, working memory

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101
Q

where is the tuberohypophyseal system located and what is it in charge of?

A

hypothalamus

prolactin release

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102
Q

what do the D1 and D5 receptors do?

A

increase cAMP

Gs coupled
stimulate adenylyl cyclase activity

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103
Q

what do D2, D3, D4 receptors do?

A

decreases cAMP

Gi coupled
inhibit adenylyl cyclase activity
increase gk, hyperpolarize

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104
Q

methylphenidate

A

catecholamine reuptake blocker

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105
Q

apomorphine

A

nonselective D1 and D2 receptor agonist

106
Q

SKF 383393

A

D1 receptor agonist

107
Q

DETQ

A

D1 receptor positive allosteric modulator

108
Q

Quinpirole

A

D2/D3 receptor agonist

109
Q

bromocroptine, pramipexole, ropinirole, rotigotine

A

D2/D3 receptor agonist

110
Q

SCH 23390

A

D1 receptor antagonist

111
Q

Haloperidol

A

D2 receptor antagonist

112
Q

DA regulates _______ along a continuum

A

behavioral activation

113
Q

reducing da synthesis ______ behavioral activation?

114
Q

what happens when reserpine blocks VMAT

A

sedation in animals
depression in humans

115
Q

what happens when AMPT blocks TH activity

A

associated with relapse into depression following positive response to antidepressant medication

116
Q

what happens following a bilateral central lesion?

A

sensory neglect
motivational deficits
parkinsonian motor deficits

117
Q

what happens after a unilateral 6-OHDA lesion to the SNpc

A

loss of DA input to lesion side, however DA continues to release behavior on intact side

118
Q

adrenergic agonists in the LH promote ______

A

wakefulness

119
Q

adrenergic input to the PFC can improve or impair _______

A

working memory

120
Q

how do a2-AR agonists like guanfacine and clonidine affect performance of delayed task resonse?

121
Q

does a1-AR have a high or low affinity for NE?

122
Q

serotonin synthesis

A

tryptophan –(TPH2/fe2+, 02, BH4)–> 5-HTP –(AADC/ vitamin B6)–> 5-HT

123
Q

what is the rate limiting step in serotonin synthessi

124
Q

what happens with TRP depletion

A

induces symptoms in people with major depression

125
Q

what does PCPA do?

A

blocks 5-HT synthesis by irreversibly inhibiting TPH

126
Q

5-HT is loaded into vesicles by ______

127
Q

what kind of receptors at 5-HT 1B/1D

A

terminal autoreceptors

128
Q

what kind of receptors are 5-HT1A receptors

A

somatodendritic

129
Q

what do 5-HT 1b/1d terminal autoreceptors do

A

inhibit 5-HT release
decrease Ca2+ influx
decrease cAMP

130
Q

what do 5-HT 1a somatodendritic autoreceptors do

A

opens K+ channels, hyperpolarizing Vm
decrease neural activity
important in psychopharmacology of SSRIs

131
Q

SERT

A

5-HT transporter

target of SSRI, cocaine, and MDMA

132
Q

MAO-A

A

enzymatic degradation

5-HIAA is major metabolite

133
Q

para-chloroamphetamine and fenfluramine

A

5-HT releaser

134
Q

MDMA

A

5-HT releaser

135
Q

buspirone

A

5-HT1a partial agonist

136
Q

what other condition is MDMA used for?

137
Q

where are majority of 5-HT neurons found in the CNS?

A

raphé nuclei

138
Q

8-OH-DPAT

A

5-HT1a full agonist

139
Q

WAY-100635

A

5-HT1a antagonist

140
Q

DOI

A

5-HT2a agonist

141
Q

LSD

A

5-HT2a agonist

142
Q

katanserin and ritanserin

A

5-HT2a antagonist

143
Q

triptans

A

5-HT1b/1d agonists

144
Q

lasmiditan

A

5-HT1f agonist

145
Q

how is territorial aggression tested on animals

A

resident-intruder tests

146
Q

impaired 5-HTergic signaling ______ behavioral aggression

147
Q

what is the 5-HT Deficiency Hypothesis

A

impaired 5-HTergic signalling increases behavioral aggression

148
Q

5-HT1a _______ are anxiolytic

A

partial agonists

149
Q

5-HT1b and 5-HT2c agonists do what to behavior?

A

reduce feeding

150
Q

what is addiction?

A

a chronic, relapsing behavioral disorder

151
Q

describe the impulsive stage of addiction cycle

A

binge intoxication
pleasurable effects
abstinence neutral affect
reward craving

152
Q

describe the compulsive stage of drug addiction

A

prolonged intoxication
relief
protracted abstinence negative affect
relief craving

153
Q

what are the rewarding properties of drug abuse

A

the positive experience associated with the drug

the “high”

154
Q

what are the positively reinforcing properties of drug abuse

A

consuming the drug strengthens whatever preceding behavior was performed

how hard an animal will work for a drug

155
Q

rewarding properties of drugs are commonly evaluated using which two animal tests?

A

place conditioning
electrical self-stimulation

156
Q

withdrawal from ethanol _____ threshold for electrical self-stimulation of reward pathway

157
Q

how is relapse to drug use modeled

A

reinstatement

158
Q

how is reinstatement performed in animals?

A

CS’s, stress, or drug exposure

159
Q

describe the impulsive stage

A

driven by positive reinforcement, drug reward properties

activation of the reward circuit

160
Q

describe compulsive stage

A

driven by negative reinforcement; removal of negative stimuli

recruitment of anti-reward circuitry

161
Q

what brain regions are in reward pathway

A

VTA
Nuc. Acc

162
Q

what brain regions are involved in antireward pathway

A

CaA, BNST
LC

163
Q

PFC dysfunction in addiction is characterized by

A

intrusive thoughts
craving
poor impulse control

164
Q

cocaine-HCl

A

oral, intranasal, IV
vulnerable to heat

165
Q

free base cocaine

A

dissolve in H2O, NaHCO3
heat & dry = “crack”

166
Q

lipophillic cocaine

A

easily crosses BBB

167
Q

metabolites for cocaine

A

benzoylecgonine
coc+EtOH –> cocaethylene

168
Q

what are the drug actions for cocaine

A

inhibit NT transporters
–high affinity for NET and SERT

increased DA release independent of DAT
–inhibition of NET in PFC drives excitation of VTA

169
Q

m/AMPH drug actions

A

enters DA nerve terminals by DAT uptake, provoking release from synaptic vesicles into cytoplasm

DAT functions in reverse, releasing DA into extracellular fluid

170
Q

what are the behavioral effects of cocaine?

A
  1. euphoric high
  2. behavioral activation (repetitive stereotyped behaviors, locomotion, rearing, sniffing)
  3. sympathetic arousal (tachycardia, vasoconstriction, hypertension, hyperthermia)
171
Q

psychostimulant microinjection into the Nuc. Acc. induces what behavioral effect?

A

increase locomotor behavior

172
Q

psychostimulant microinjection into dorsal striatum induces what behavioral effect?

A

increase stereotyped behaviors

173
Q

6-OHDA lesion in Nuc. Acc induces which behavioral effect?

A

decreased locomotor

174
Q

6-OHDA lesion in dorsal striatum induces which behavioral effect?

A

decreased stereotyped behaviors

175
Q

true or false: COC-insensitive DAT-ki mice do not self-administer cocaine

176
Q

Do D1 KO mice self-administer cocaine?

177
Q

do D2 or D3 KO mice self-administer cocaine?

178
Q

once-daily, intermittent administration of cocaine results in _______

A

sensitization

179
Q

continuous cocaine administration results in _______

180
Q

what does chronic cocaine use do to the brain?

A

decreased gray matter volume

hypofunction of PFC

181
Q

what are the names of natural opiates?

A

morphine, codeine, thebaine

182
Q

postsynaptic inhibition of endogenous opioids

A

opens k+ channels

183
Q

axoaxonic inhibition of endogenous opioids

A

close Ca2+ channels

184
Q

presynaptic inhibition of endogenous opioids

A

reduce transmitter release

185
Q

what are the PNS effects of opioids?

A

pinpoint pupils
vomiting
cough suppression
constipation

186
Q

how does death by opioids occur?

A

respiratory depression
cardiac depression

187
Q

what are the three symptoms of “opioid overdose triad”

A

pinpoint pupils, unconsciousness, respiratory depression

188
Q

what do 6-OHDA lesions do to self-administration for opioids?

A

reduce, but not stop completely

189
Q

injection of naloxone into which brain structure produces the physiological symptoms of WD?

190
Q

injection of naloxone into which brain structure produces the aversive properties of WD?

191
Q

ethanol synthesis

A

alcohol –(alcohol dehydrogenase/NAD)–> acetaldehyde –(aldehyde dehydrogenase/NAD)–> acetic acid –(oxidation reaction)–> carbon dioxide

192
Q

in acute tolerance, effects of alcohol are _____ during the elimination phase

193
Q

how does EtOH interact w GABA receptors?

A

increases Cl- flux through GABAa receptors

194
Q

how does EtOH interact w glutamate receptors?

A

EtOH inhibits iGlu receptors, decreasing release.

195
Q

how do blackouts occur?

A

acute EtOH inhibits NMDA receptors and decreases LTP

196
Q

what is wet brain

A

EtOH induced excitotoxic damage

197
Q

chronic EtOH associated with _____ of alpha1 and ______ of alpha 4 and 6

A

down-regulation
up-regulation

198
Q

what are the two THC metabolites?

A

11-OH-THC
THC-COOH

199
Q

what is the half life of THC

A

20-30 hours

200
Q

what are the two endocannabinoids

A

anandamide
2-AG

201
Q

anandamide

A

CB1 partial agonist
degraded by FAAH

202
Q

2-AG

A

full, nonselective CB1 and 2 agonist
degraded by MAGL

203
Q

what converts DAG to 2-AG

A

DAG Lipase

204
Q

retrograde signaling by endocannabinoids is involved in ______

A

synaptic plasticity

205
Q

what are CP-55,940 and WIN 55,212-2

A

full CB1 and 2 agonists

206
Q

what is SR 141716A

A

selective CB1 antagonist

207
Q

what is Epidiolex

A

first FDA-approved drug that contains a purified drug substance derived from cannabis

–lennox-gastaut syndrome
–dravet syndrome

208
Q

CB1-R in VTA

A

hyperpolarize IN
decrease GABA release
increase VTA firing
increase dopamine release

209
Q

prazosin

A

alpha1-AR antagonist

increases peripheral vasodilation

reduces nightmares in PTSD

210
Q

propranolol

A

beta-AR antagonist

negative chronotropic and negative ionotropic effects on heart

reduces performance anxiety in social anxiety disorder

211
Q

5-HT1a autoreceptors

A

dorsal and median raphé

inhibit neuronal firing and 5-HT release

agonists are anxiolytic

212
Q

5-HT postsynaptic receptors

A

hippocampus and amygdala

emotional and cognitive aspects

agonists are anxiogenic

213
Q

short allele

A

smaller amygdala and sgACC volume

increased amygdala activity

greater symptom severity in anxiety disorders

214
Q

early elevated 5-HT

A

short allele is low-expressing

SERT KO are more anxious

215
Q

what are benzodiazepines

A

positive allosteric modulators of GABA a receptors

216
Q

long-acting BZD

A

metabolites are psychoactive

librium

valium

217
Q

short(er)-acting BZD

A

metabolized in one step

xanax

ativan

klonopin

218
Q

short-acting BZD

A

rohypnol

versed

219
Q

neurontin and Lyrica

A

anticonvulsants

block active calcium channels

reduces excitatory neurotransmission

off-label use

220
Q

how to view anhedonia in animal models

A

sucrose preference

221
Q

how to view anxiety in animal models

A

novelty-suppressed feeding

222
Q

what is the specific action of TCAs

A

inhibit NET and SERT

223
Q

what are the HAM side effects and how are they caused?

A

***caused by off-target sites antagonism

H1- sedation/fatigue, weight gain

a-AR - hypotension, arrhythmia

mACh - dry mouth, constipation, dizzy

224
Q

fluoxatine

A

“activating”

5-HT2c antagonist

225
Q

sertraline

A

“activating”

DAT blockade

226
Q

paroxetine

A

anxiolytic

NET blocker

anti-cholinergic

227
Q

lexapro

A

the purest SSRI

228
Q

trazodone and nefazodone

A

multi-action AD, used for sedative properties

serotonin antagonist and reuptake inhibitor

sedating (H1) effective in insomnia

antagonism reduces SSRI side effects, though priapism is possible

229
Q

effexor

A

SNRI

selectively boosts DA in PFC

230
Q

duloxetine

A

SNRI

AD in absence of pain

231
Q

fetzima

232
Q

which two dual-action ADs have the lowest incidence of sexual dysfunction?

A

wellbutrin and mirtazapine

233
Q

viibryd

A

5-HT1a partial agonist

234
Q

trintellix

A

5-HT1a antagonist

235
Q

zulresso

A

PPD

positive modulator for GABAa receptors

continuous IV infusion over 60 hours

236
Q

spravato

A

nasal spray used in conjunction w AD

237
Q

acute AD administration _____ release of 5-HT

238
Q

ketamine

A

non-competitive NMDA receptor antagonist

239
Q

what is necessary for ketamine to be an effective AD?

A

dendritic spines

240
Q

what is the name of the phenothiazine

A

chlorpromazine

241
Q

what is the name of a butyrophenone

A

haloperidol

242
Q

describe neuroleptics

A

D2 receptor antagonists

effective antipsychotics

significant side effects

**EFFECTIVE IN TREATING POSITIVE SYMPTOMS

243
Q

nigrostriatal pathway function w neuroleptics

A

EPS side effects

244
Q

meso-limbic pathway function w neuroleptics

A

antipsychotic efficacy

245
Q

tubero-hypophyseal pathway function w neuroleptics

A

endocrine side effects

246
Q

clozapine

A

effective atypical antipsychotic for 1/3 people non-responsive to neuroleptics

EPS side effects are less severe

reduces risk of suicide

247
Q

side effects of clinical use of clozapine

A

loss of WBCs

substantial weight gain

reduced seizure threshold

248
Q

what do atypical antipsychotics have high affinity for

A

5-HT2a antagonists

249
Q

2 pips and a rip

A

D2 partial agonist
5-HT1a partial agonist

adjunct in MDD
abilify
rexulti

250
Q

peens and dones

A

depressive episodes in BD
quetiapine
lurasidone

251
Q

T/F: CRF acts as both a hormone and a neurotransmitter

252
Q

T/F: inhibitions of the LC can elicit alerting and fear responses in animals

253
Q

T/F: the role of serotonin is not entirely clear bc some serotonin receptor subtypes can have opposite effects on anxiety

254
Q

T/F: barbiturates are not commonly used for the treatment of insomnia bc they can induce dependence and can be lethal in overdose

255
Q

T/F: some BZD, such as valium and librium, are long-acting anxiolytics bc they have active metabolite

256
Q

In general, the addiction potential of a drug is positively correlated with its

a. duration of action
b. speed of onset
c. ability to cause relapse
d. all of the above

A

b. speed of onset

257
Q

T/F: drug self administration studies typically produce a dose-response curve that is sigmoid shape

258
Q

an increased threshold for electrical self-stimulation during withdrawal from alcohol is generally interpreted to indicate a(n)

a. state of intoxication
b. increase sensitivity of the reward circuit
c. state of craving
d. decrease in sensitivity of the reward circuit

A

d. decrease in sensitivity of the reward circuit

259
Q

Koob and Le Moal propose that after repeated bouts of intoxication and withdrawal, drug use is driven by

a. rewarding properties of the drug
b. negative reinforcement
c. prefrontal cortex deficits
d. the reward circuitry

A

b. negative reinforcement

260
Q

which of the following structures are part of the proposed circuitry involved in the rewarding and reinforcing effects of abused drugs?

a. amygdala
b. PFC
c. nuc. acc.
d. ventral pallidum
e. all of the above

A

e. all of the above