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PSYC 336 - Drugs and Behavior > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

encephalon

A

the brain

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2
Q

structures in the forebrain

A

telencephalon, diencephalon

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3
Q

structures in the telecephalon

A

neocortex, basal ganglia, limbic system

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4
Q

structures in the diencephalon

A

thalamus, hypothalamus

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4
Q

mesencephalon

A

midbrain

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5
Q

structures in the hindbrain

A

metencephalon, myelencephalon

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6
Q

structures in the metencephalon

A

cerebellum, pons

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7
Q

myelencephalon

A

medulla

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8
Q

brainstem

A

midbrain, pons, medulla

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9
Q

major striatum components

A

nucleus accumbens, caudate nucleus, putamen

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10
Q

caudate nucleus

A

dorsomedial striatum

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11
Q

putamen

A

dorsolateral striatum

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12
Q

function of nucleus accumbens (core and shell)

A

pleasure, motivation, reward cues

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13
Q

major target of dopamine axon terminals

A

striatum

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14
Q

dopamine neurons in the striatum

A

no DA neurons in the striatum; cell bodies are in the brainstem and send axon projections into the striatum

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15
Q

monoamine neurons

A

dopamine, serotonin, norepinephrine

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16
Q

monoamine neurons in the brain

A

primarily in the brainstem; cell bodies in the brainstem and send axon projections throughout the brain

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17
Q

dopamine neuron locations

A

in the substantia nigra and ventral tegmental area

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18
Q

nigrostriatal pathway

A

dopamine neurons in the substantia nigra send axon projections to the dorsal striatum

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19
Q

mesolimbic pathway

A

dopamine neurons in the VTA send axon projections to the nucleus accumbens and amygdala

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20
Q

mesocortical pathway

A

DA neurons in the VTA send axon projections into the prefrontal cortex

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21
Q

basal ganglia circuits/loops are important for:

A

voluntary movement, action selection, procedural learning, habits

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22
Q

input structures for the basal ganglia

A

cortex; glutamatergic/excitatory

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23
Q

output structures for basal ganglia

A

GPi, SNr; GABAergic/inhibitory

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24
Q

striatum projections are…

A

GABAergic

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25
Q

direct striatum projection

A

excites target of basal ganglia output, “go”

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26
Q

indirect striatum projection

A

inhibits targets of basal ganglia output, “no-go”

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27
Q

feedback for basal ganglia

A

provided by thalamus and midbrain dopamine

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28
Q

GABA neurons in striatum

A

half express D1 receptor, half express D2

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29
Q

D1 neurons

A

part of direct pathway “go,” excited by dopamine

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30
Q

D2 neurons

A

part of the indirect pathway, “no-go,” inhibited by dopamine

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31
Q

common property of addictive drugs

A

increase dopamine (but through different mechanism)

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32
Q

components of reward learning

A

liking, wanting, reward prediction

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33
Q

liking

A

pleasurable aspect of reward, does not involve dopamine

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34
Q

wanting

A

motivational drive to work for rewards, involves DA

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35
Q

reward prediction

A

involves DA

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36
Q

reward prediction: unexpected reward

A

increase in DA firing

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37
Q

reward prediction: response to CS

A

increase in DA firing when CS presented, not the reward itself

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38
Q

reward prediction: CS + no reward

A

decrease in DA firing

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39
Q

positive prediction error

A

reward is greater than expected

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40
Q

negative prediction error

A

reward is less than expected

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41
Q

positive prediction error effects

A

activates D1 cells (Gs coupled) and direct pathway

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42
Q

negative prediction error effects

A

activates D2 cells (Gi coupled) and indirect pathway

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43
Q

properties of a drug that can cause addiction

A
  • route of administration

- increased lipid solubility

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44
Q

individual differences that can cause addiction

A

genes, environment, and the interaction between the two

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45
Q

genetic factors that increase addiction likelihood

A
  • high impulsivity

- history of stress or trauma

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46
Q

genetic factor that decreases addiction likelihood

A

environmental enrichment

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47
Q

impulsivity in meth abusers

A

decreased D2 receptor availability in the striatum correlated with higher impulsivity

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48
Q

impulsivity in rats

A

high level of premature responding shows decreased D2 binding in ventral striatum

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49
Q

impulsivity and cocaine

A

high-impulsivity rats will self-administer more cocaine; indicated impulsivity may be a pre-existing condition for addiction

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50
Q

stress

A

influences all aspects of addiction process (drug taking, vulnerability to addiction, relapse)

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51
Q

stress: enhanced vulnerability

A

history of social defeat stress shows enhanced place preference for low-dose cocaine

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52
Q

environmental enrichment

A

reduced conditioned place preference for cocaine

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53
Q

prefrontal cortex (PFC)

A

behavioral inhibition, self-control, executive function

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54
Q

nucleus accumbens (ventral striatum)

A

reward, motivation, cues

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55
Q

dorsomedial striatum (DMS)

A

goal-directed learning

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56
Q

dorsolateral striatum (DLS)

A

habit learning

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57
Q

habit behavior is what type of association?

A

stimulus-response association

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58
Q

goal directed behavior is what type of association?

A

response-outcome association

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59
Q

chronic stress causes:

A
  • enhanced habit learning
  • loss of PFC volume
  • reduced dendritic complexity
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60
Q

chronic stress affects striatum:

A

changes neuronal density in dorsal striatum → DLS more dominant that DMS

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61
Q

drug-induced neural adaptations

A
  • sensitization of drug effects
  • enhanced habit learning
  • reduced behavioral inhibition
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62
Q

enhanced drug motivation experiment

A

intermittent cocaine use followed by abstinence → increased cocaine potency and drug motivation

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63
Q

habit learning

A

history of cocaine exposure to habitual learning

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64
Q

behavioral inhibition: resistance to negative consequences

A

some rats continue to self-administer cocaine despite getting footshock, resistant to punishment

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65
Q

behavioral inhibition: role for PFC

A
  • optogenetic stimulation of PFC restores sensitivity to footshock
  • optogenetic inhibition of PFC makes animals resistant to footshock
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66
Q

drug class of cocaine and amphetamines

A

stimulants/psychostimulants/psychomotor stimulants/uppers

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67
Q

drugs in stimulant category

A

cocaine, amphetamines, nicotine, caffeine

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68
Q

properties of cocaine

A
  • psychoactive alkaloid

- weak base

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69
Q

natural form of cocaine

A
  • raw coca leaf chewed with lime/ash to increase saliva pH (enhances absorption)
  • < 2% cocaine
  • absorbed in mouth
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70
Q

cocaine in 1800s and early 1900s

A

widely used; doctors and scientists highly praised its properties

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71
Q

coca paste

A
  • crude extraction from leaves
  • ~80% cocaine sulfate
  • can only be smoked
  • aka “paco” or “basuco”
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72
Q

cocaine HCl

A
  • crystalline powder
  • extracted and purified from coca paste
  • very high concentration
  • water soluble
  • can be taken orally, intranasally, or intravenously; CANNOT be smoked
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73
Q

cocaine free base

A
  • made from cocaine HCl + water + base
  • vaporized and smoked (“freebasing”)
  • residual can be dangerous and explode with flame
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74
Q

crack cocaine

A
  • made from cocaine HCl
  • baking soda instead of solvent, making it safer
  • 75-90% cocaine
  • smoked
  • led to new cocaine epidemic in 80s-90s
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75
Q

cocaine products

A

widely used in many products in the 1800s

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76
Q

current medical uses for cocaine

A

local anesthetic effects (Schedule II)

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77
Q

effects at high doses of cocaine (in the brain)

A

inhibits voltage-gated Na+ channels (involved in action potentials)

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78
Q

cocaine absorption and distribution

A

extremely rapid absorption with smoking/IV

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79
Q

peak subjective effects for crack cocaine

A

within ~1-2 mins

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80
Q

inactive major metabolite in cocaine

A

benzoylecgonine

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81
Q

half-life of cocaine

A

0.5-1.5 hrs

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82
Q

active metabolite in cocaine

A

cocaethylene; formed when cocaine and ethanol are ingested simultaneously

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83
Q

amphetamines

A

chemical family of synthetic and natural psychostimulants

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84
Q

ephedrine

A
  • comes from ephedra or “mormon tea” plant (natural)
  • active components: ephedrine and pseudoephedrine
  • decongestants
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85
Q

cathinone

A
  • comes from “qat” or “khat” shrub leaves (natural)

- commonly chewed

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86
Q

bath salts

A
  • synthetic variant of cathinone
  • methcathinone (“cat”) and mephedrone (“meow meow”)
  • designer drugs
  • DEA schedule I
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87
Q

timeline of use of amphetamines and methamphetamines

A

1920s-30s: medical use developed
40s: widespread adoption b/c of WWII
early 70s: peak use of “speed”

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88
Q

first uses of amphetamines/methamphetamines

A
  • benzadrine inhaler (for congestion)

- narcolepsy

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89
Q

forms of synthetic amphetamines

A

D-Amphetamine, L-Amphetamine, Adderall

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90
Q

route of administration for synthetic amphetamines

A

typically orally or injection (IV, SC)

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91
Q

methamphetamines (synthetic)

A

most potent of amphetamines

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92
Q

route of administration for methamphetamines

A

oral, snorted, injected IV, or smoked

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93
Q

amphetamine-related synthetics

A
  • differ in chemical structure

- methylphenidate, modafinil

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94
Q

previous uses for amphetamine

A
  • congestion
  • mood and weight control
  • fatigue
  • increase attention and decrease fatigue in military
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95
Q

meth epidemic

A
  • easily prepared in common household ingredients
  • greater abuse potential
  • can be smoked
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96
Q

current medical uses for amphetamines

A
  • narcolepsy

- ADD/ADHD

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97
Q

metabolism and excretion of amphetamines

A
  • slower metabolism and elimination compared to cocaine

- half-life is 7-30 hours

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98
Q

stimulants: major effects

A
  • mild to moderate: heightened energy, hyperactive ideation, anger, verbal aggression, inflated self-esteem, etc.
  • severe: total insomnia, rambling, incoherent speech, possible extreme violence, delusions of grandiosity
  • autonomic effects: increased BP, hyperthermia, bronchodilation
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99
Q

cocaine vs amphetamines: duration of action

A

cocaine has a shorter duration of action

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100
Q

cocaine vs amphetamines: cardiovascular effects

A

cocaine has worse cardiovascular effects, can be lethal

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101
Q

cocaine vs amphetamines: seizures

A

higher convulsive seizure properties in cocaine

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102
Q

major effects of stimulants in animals

A
  • locomotor activity can appear to decrease with high AMPH doses because rats perform with stereotypy behavior instead
  • reinforcing/rewarding effects
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103
Q

effects of withdrawal

A

mostly psychological, especially in chronic, high-dose users

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104
Q

tolerance to some effects of psychostimulants

A

autonomic and anorexic effects

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105
Q

sensitization to other effects of psychostimulants

A

rewarding effects, psychotomimetic effects (psychosis), locomotor stimulant effects

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106
Q

negative effects of chronic amphetamine use

A

psychosis, anorexia, physical damage

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107
Q

history of MDMA

A
  • never used clinically
  • can enhance communication and openness
  • club drug in 80s-90s
  • Schedule I
  • taken orally; long-half life (8 hrs)
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108
Q

MDMA effects at low doses

A
  • increased empathy and sociability/empathy; mild euphoria

- increased heart rate and temperature

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109
Q

MDMA effects at high doses

A
  • mild hallucinogenic effects

- hyperthermia and dehydration, increased heart rate and blood pressure can lead to stroke

110
Q

cocaine as an indirect agonist

A

blocks reuptake of monoamines (DA, NE, 5-HT)

111
Q

amphetamines as indirect agonists

A
  • cause vesicles to release transmitter
  • cause monoamines to be transported out of neuron via reversal of transporter
  • results in very high DA in synaptic cleft
112
Q

categories of monoamines

A

catecholamines and indolamines

113
Q

catecholamines

A

dopamine, norepinephrine, epinephrine

114
Q

indolamines

A

serotonin only

115
Q

tyrosine

A

precursor for catecholamines

116
Q

tyrosine hydroxylase

A

rate-limiting step in catecholamine synthesis

117
Q

all monoamines are one type of neurotransmitter

A

classical

118
Q

catecholamines are inactivated by

A
  • reuptake via transporters

- enzymatic degradation

119
Q

catecholamine reuptake

A
  • primary mechanism for inactivation

- much faster than metabolism

120
Q

vesicular monoamine transporter VMAT2

A

packages all monoamines into vesicles

121
Q

each monoamine has their own…

A

synaptic transporters and receptors

122
Q

enzymes involved in catecholamine metabolism

A

MAO and COMT

123
Q

D1-like receptors

A

D1 and D5, coupled to Gs

124
Q

D2-like receptors

A

D2, D3, D4; coupled to Gi

125
Q

presynaptic autoreceptors are mostly what type of receptor

A

D2

126
Q

area dopamine receptors are primarily concentrated

A

prefrontal cortex areas

127
Q

monoamine systems

A

a few thousand neurons in each system send broad, diffuse projections to large areas of the forebrain

128
Q

where the majority of dopamine neurons can be found

A

substantia nigra and VTA (midbrain)

129
Q

nigrostriatal pathway

A

DA neurons in substantia nigra target dorsal striatum

130
Q

mesolimbic pathway

A

DA neurons in VTA target ventral striatum (nucleus accumbens) and amygdala

131
Q

mesocortical pathway

A

DA neurons in VTA target prefrontal cortex

132
Q

dopamine in the striatum

A

no DA neurons, but has lots of DA fibers, DA release at synapses, and DA receptors/transporters

133
Q

classification of dopamine receptors in striatum

A

half D1, half D2

134
Q

cause of parkinson’s disease

A

progressive death of midbrain dopamine neurons and their striatal terminals

135
Q

symptoms of parkinson’s

A
  • bradykinesia (slow movement)

- akinesis (frozen) in severe cases

136
Q

L-DOPA

A

can relieve symptoms, but can lead to dyskinesias and other problems

137
Q

drug-induced parkinson’s disease

A
  • MPPP+ is a potent DA neurotoxin that can cause parkinson’s symptoms within days
  • converts MPTP to MAO-B
138
Q

MPTP research

A

used to produce dopamine lesions in non-human primates

139
Q

catecholamine neurotoxin

A

6-OHDA used instead of MPTP to create lesions of catecholamine neurons and/or axon fibers

140
Q

drugs that affect DA system

A

DOPA, 6-OHDA, amphetamine, cocaine, methylphenidate

141
Q

antischizophrenia drugs

A

D2 antagonists that cause sedation and cataplexy at higher doses

142
Q

4 primary adrenergic receptors are what type of receptor?

A

all GPCRs

143
Q

alpha-1 adrenergic receptor

A

coupled to Gq

144
Q

alpha-2 adrenergic receptor

A

coupled to Gi, serves as autoreceptor

145
Q

beta-1 and beta-2 adrenergic receptors

A

coupled to Gs

146
Q

locus coeruleus

A

major source of NE in the brain, neurons have TH and DBH

147
Q

dorsal noradrenergic bundle (DNAB)

A
  • originates from locus coeruleus
  • major source of NE in the brain
  • involved in cognition, arousal, and attention
148
Q

ventral noradrenergic bundle (VNAB)

A
  • originates from NE neurons in the medulla

- involved in aversive aspects of stress

149
Q

role of NE in stress and arousal

A

responsible for many stress effects on memory and cognition

150
Q

distribution of NE

A
  • central nervous system (brain)

- major components of peripheral sympathetic nervous system “fight or flight” response

151
Q

pharmacodynamics of amphetamine

A

amph, meth, and MDMA are all agonists of TAAR1 (intracellular GPCR)

152
Q

distribution of cocaine in the human brain

A

matches that of DA transporters (DAT), which are densest in the striatum

153
Q

DA is critical for…

A

the reinforcing and locomotor effects of cocaine and amphetamines

154
Q

antagonists that disrupt amphetamine reinforcement (self-administration)

A

DA, but not NE

155
Q

drugs not readily self-administered by animals or abused by people

A
  • selective blockers of NET
  • selective blockers of SERT
  • other local anesthetics (Na+ channel blockers)
156
Q

DAT blockade

A

appears to be the core mechanism by which cocaine and amphetamine are reinforcing

157
Q

lesion studies

A

using 6-OHDA to lesion DA, but not NE, disrupts cocaine reinforcement (self-administration)

158
Q

similar time course for amphetamine effects on:

A
  • DA release in striatum

- locomotor effects

159
Q

repeated amphetamine treatment

A
  • produces sensitization of locomotor and reinforcing effects
  • sensitization of DA levels in striatum
160
Q

DAT knockout mice

A
  • spontaneously hyperactive

- show increased locomotion

161
Q

DAT knock-in mice

A
  • mutation that makes them DAT insensitive to cocaine

- show loss of cocaine reinforcement (self-administration)

162
Q

Stimulant-induced DA in nucleus accumbens (mesolimbic)

A

locomotion & reinforcement

163
Q

Stimulant-induced DA in dorsal striatum (nigrostriatal)

A

stereotypies

164
Q

reward cues and dopamine

A
  • once learned, CS/reward-associated cues will elicit DA release
  • drive motivation for reward
165
Q

Cue-induced dopamine release in dorsal striatum

A

correlates with craving in addicts

166
Q

in rats, cocaine-associated cues trigger…

A

drug seeking

167
Q

treatments for stimulant addiction

A
  • no clinically licensed treatment

- best treatments are psychosocial, CBT, relapse prevention therapy

168
Q

neurotoxicity with amphetamines

A

Can cause depletion of monoamines and degeneration of nerve terminals

169
Q

Amphetamine/methamphetamine neurotoxicity:

A
  • high doses (10-50x)
  • high extracellular DA necessary
  • amphetamine: damage to DA terminals
  • methamphetamine: damage to DA and 5-HT terminals
170
Q

MDMA neurotoxicity

A
  • only 2x normal street dose

- damage to 5-HT terminals

171
Q

methamphetamine neurotoxicity in humans

A

Long-lasting decrease in DAT availability in abstinent methamphetamine and methcathinone users

172
Q

methamphetamine neurotoxicity in baboons

A

Long-lasting decrease in DAT availability after meth

173
Q

methamphetamine neurotoxicity in rats

A

Long-lasting decreases in TH and DAT after meth

174
Q

acute adverse effects of MDMA

A
  • reflect dehydration and hyperthermia

- subtle cognitive deficits

175
Q

properties of sedative-hypnotics

A
  • depress the CNS and behavior
  • anxiolytic properties (downers)
  • addictive effects
  • cross-dependence and -tolerance
176
Q

types of sedative-hypnotics

A

alcohol, barbiturates, benzodiazepines

177
Q

structurally unrelated drugs similar to sedative-hypnotics

A

nonbenzodiazepines, methaqualone, GHB, opiates/opioids

178
Q

properties of alcohol

A
  • ethanol (ethyl alcohol) is consumed
  • other forms are too toxic
  • no current medical use
  • not scheduled by the DEA
179
Q

forms of alcohol: fermentation

A
  • natural source

- yeast fermentation only produces concentrations up to 15%

180
Q

forms of alcohol: distillation

A
  • produces spirits or hard liquor

- concentration >15%

181
Q

history of alcohol use

A
  • incidence of alcohol abuse increased with distillation
  • repeated attempts to ban it (temperance movement, prohibition)
  • attempt to ban had opposite intended effects
182
Q

alcohol molecules are ionized/non-ionized

A

non-ionized

183
Q

% of alcohol absorbed and where

A

10% absorbed in stomach, 90% in small intestine

184
Q

presence of food in stomach & it’s affect on alcohol absorption

A
  • food in stomach slows gastric acid emptying and absorption

- more alcohol is degraded before being absorbed (first-pass metabolism)

185
Q

small amounts of alcohol eliminated without being transformed

A

roughly 10% in sweat, tears, urine, and breath

186
Q

breath levels are usually a good indicator of…

A

blood levels

187
Q

how most alcohol is broken down

A

alcohol dehydrogenase (ADH) in stomach and liver

188
Q

ADH (alcohol dehydrogenase) individual differences

A
  • affects blood levels of alcohol

- 60% more gastric ADH in men

189
Q

ALDH individual variation

A
  • affects blood levels of acetaldehyde

- 50% of certain Asian groups have reduced ALDH function

190
Q

alcohol excretion

A

zero-order kinetics, cleared at a constant rate

191
Q

blood alcohol content (BAC/BEC)

A

grams of alcohol per 100 mL of blood

192
Q

person with BAC of 0.2-0.3

A

quite drunk

193
Q

person with BAC 0.45

A

LD50 (death), low margin of safety

194
Q

cause of death from alcohol

A

respiratory centers in the brainstem shut down

195
Q

alcohol effects on drunk driving

A
  • increased probability of car accidents
  • impaired reaction time and judgment
  • increased aggression
196
Q

alcohol effects: increased blood circulation

A

blood vessels dilated, feeling of warmth

197
Q

alcohol effects: anti-diuretic hormone

A

ADH (anti-diuretic hormone) inhibited = increased urination and dehydration

198
Q

alcohol effects: sleep

A

impairs REM sleep

199
Q

alcohol effects: memory

A

blackouts/amnesia

200
Q

alcohol effects on vestibular system

A
  • alcohol makes blood less dense, which changes density of cupula compared to surrounding fluid
  • sensation of movement triggers vestibular-ocular reflex
201
Q

cupula

A

in semicircular canals (part of vestibular system in inner ear), senses movement

202
Q

alcohol withdrawal: hangover

A

seen as a mini-withdrawal

203
Q

alcohol withdrawal: chronic use

A
  • can be fatal
  • seizures, hallucinations, tremors, autonomic disruption
  • treated using benzos because of cross-dependence
204
Q

acute tolerance of alcohol

A
  • aka tachyphylaxis

- ascending and descending BAC

205
Q

metabolic tolerance of alcohol

A
  • increased expression of ADH

- induction of liver enzymes of cytochrome P450 family

206
Q

other types of alcohol tolerance

A

behavioral, pharmacodynamic, cross-tolerance with benzos/barbs

207
Q

negative effects of chronic heavy alcohol use

A
  • liver damage (~10-20%)

- brain damage, including Korsakoff syndrome

208
Q

fetal alcohol syndrome

A
  • alcohol readily crosses placenta
  • lower birth body weight
  • craniofacial malformations
  • neurological problems
  • binge drinking and high BAC have been implicated in FAS
209
Q

risks for alcoholism

A
  • stress
  • lifetime anxiety
  • early-life stress
  • increased novelty seeking
  • family history of alcoholism
210
Q

self-administration of alcohol in animals

A
  • most animals will drink only a little alcohol

- selective breeding –> populations that drink more alcohol or abstain completely

211
Q

forms of barbiturates

A
  • comes from barbituric acid (synthetic)

- barbital and phenobarbital were first drugs to be marketed

212
Q

barbiturate uses (overall)

A
  • anxiolytics, hypnotics, and anticonvulsants

- “truth serum”

213
Q

medical use for barbiturates

A
  • anesthesia
  • sedation
  • epilepsy
214
Q

risks of barbiturates

A

significant addiction potential and overdose risk

215
Q

drug that replaced barbs

A

benzos

216
Q

retired uses of barbs

A
  • sleep induction
  • anxiety
  • alcohol withdrawal (too dangerous)
217
Q

DEA schedule for barbs

A

II, III, IV

218
Q

side effects of barbs

A
  • reduced REM sleep and slow wave sleep
  • reduced cognitive function
  • dangerous with alcohol
  • tolerance –> dose escalation –> reduced margin of safety
  • dependence and withdrawal (seizures)
219
Q

barbiturate abuse

A

used recreationally to relieve anxiety, decrease inhibition

220
Q

barbiturate effects at high doses

A

respiratory centers in the brainstem shut down, common means of suicide

221
Q

use of benzodiazepines

A
  • anxiolytics
  • sedatives
  • anticonvulsants
  • treatment for alcohol withdrawal
  • surgical sedation/amnesia
222
Q

duration of action for benzos

A

varies for different benzos due to

  • depot binding
  • metabolic pathways (active vs inactive metabolites)
223
Q

properties of nonbenzodiazepines

A
  • similar benefits, side effects, and risks

- different chemical structure from benzos

224
Q

use for nonbenzos

A

sleep disorders

225
Q

pharmacodynamic properties of nonbenzos

A

act at the binding site of GABAa receptors

226
Q

medical uses of benzos

A
  • schedule IV
  • anxiety
  • emotional stress
  • relief from agitation and alcohol withdrawal
  • sedation
  • pre-surgery relaxation & anterograde amnesia
  • anticonvulsant
  • amnesia (roofies)
227
Q

safety of benzos compared to barbs

A
  • less metabolic tolerance
  • lower dependence and abuse
  • higher therapeutic index; do not affect respiratory centers in brain
  • much harder to take a lethal overdose of benzos
228
Q

reversal agent for benzos

A

Flumazenil, competitive antagonist for benzos

229
Q

abuse of benzos

A

less liable to be abused by humans than barbs

230
Q

dependence/withdrawal of benzos

A
  • milder form of alcohol/barbiturate withdrawal symptoms

- persistent emotional disturbances following withdrawal

231
Q

other forms of abuse for benzos

A

Rohypnol (date rape drug)

232
Q

DUI dangers of benzos

A
  • sleep medications (Ambien) can leave people drowsy in the morning
  • possibility of “sleep driving”
233
Q

anxiolysis of barbs/benzos

A
  • both are anxiolytic in animals and humans
234
Q

pharmacodynamics of sedative-hypnotics

A

enhance chloride influx through GABAa receptors (ionotropic)

235
Q

pharmacodynamics of barbs/benzos

A

unique binding sites on GABAa receptors

236
Q

pharmacodynamics of alcohol

A

unknown mechanism at GABAa receptor

237
Q

similarities of alcohol to barbs/benzos

A
  • similar spectrum of behavioral effects
  • similar increase in chloride currents
  • cross-tolerance and cross-dependence
238
Q

quaaludes

A

originally used as a hypnotic, sedative, or muscle relaxant

239
Q

use of GHB

A
  • decreased use now due to abuse potential
  • subjective effects of GHB mostly resemble alcohol
  • mild stimulant-like effects
  • Xyrem for narcolepsy/cataplexy
240
Q

abuse of GHB

A

club drug and date-rape drug

241
Q

mechanism of action for GHB

A

acts as an agonist for GHB receptor and GABAb receptor (both GPCRs)

242
Q

GABAb vs GHB receptor in response to GHB

A

GABAb receptor primarily involved in behavioral effects of GHB

243
Q

GHB: GABAb knockout mice

A

do not display typical behavior or physiological effects to GHB

244
Q

GHB: GHB receptors in mice

A

normal mice don’t respond to a selective agonist for GHB receptor

245
Q

GABA in the brain

A
  • most important inhibitory neurotransmitter in the adult, vertebrate brain
  • found throughout brain in high concentrations (many neurons and nuclei)
  • important role in regulating excitation
246
Q

GABA synthesis

A

GABA is formed from glutamate (immediate precursor) via enzyme glutamic acid decarboxylase (GAD)

247
Q

VGAT stands for…

A

vesicular GABA transporter

248
Q

GABA transporters

A

GAT-1, GAT-2, GAT-3 (on neurons and glia); transports GABA out of synapse

249
Q

GABA metabolism/degradation

A

via the enzyme GABA amino-transferase (GABA-T)

250
Q

GABAa receptors

A
  • ionotropic
  • ligand-gated Cl- channels
  • 5 subunits (2 alpha, 2 beta, 1 gamma)
251
Q

GABAb receptors

A
  • metabotropic
  • need two different subunits
  • autoreceptor
252
Q

GABA binding to GABAa

A

increased Cl- conductance –> hyperpolarization and IPSPs

253
Q

mechanism of action for barbs/benzos

A
  • act at different site of GABAa receptors

- act at a different site than GABA

254
Q

mechanism of action for all sedative-hypnotics

A

enhance chloride influx through GABAa receptors

255
Q

benzo effects of GABA transmission

A
  • cause GABAa channels to open more frequently

- need GABA; benzos have no effect alone, benzos are positive allosteric modulators

256
Q

barb effects of GABA transmission

A
  • cause GABAa channels to stay open for longer durations

- barbs have some direct agonist effects without GABA

257
Q

benzo binding site

A
  • discovered in 1977

- benzo binding correlates with anxiolytic effects

258
Q

benzo inverse agonists (beta-carbolines)

A
  • beta-carbolines negatively modulate GABAa receptor

- found in psychedelic drug ayahuasca

259
Q

GABAa subunits: benzo behavioral effects

A

GABAa receptors with different subunits are differentially involved in various behavioral effects of benzos

260
Q

alpha2 subunit: anxiolytic effects on benzos

A

anxiolytic effects require alpha2-conditioning GABAa receptors

261
Q

alpha1 subunit: rewarding effects of benzos

A
  • rewarding effects require alpha1-containing GABA receptors

- increase firing of VTA dopamine neurons via disinhibition

262
Q

low to moderate effects of alcohol

A

specific, acute effects

263
Q

high doses of alcohol

A

nonspecific effects

264
Q

acute effects of alcohol on glutamate mechanisms

A
  • inhibits glutamate transmission
  • reduces effectiveness of glutamate actions at NMDA receptor
  • results in memory loss
265
Q

chronic effects of alcohol on glutamate mechanisms

A
  • upregulation of NMDA receptors

- hyperexcitability during withdrawal

266
Q

acute effects of alcohol on GABA mechanisms

A

increases GABA-induced Cl- influx at GABAa receptor

267
Q

chronic effects of alcohol on GABA mechanisms

A
  • reduces GABAa-mediated Cl- influx

- hyperexcitability during withdrawal

268
Q

acute effects of alcohol on DA mechanisms

A
  • increases DA transmission

- alcohol self-administration reduced, but not blocked, by DA antagonist or 6-OHDA lesions

269
Q

chronic effects of alcohol on DA mechanisms

A
  • reduction in DA transmission

- withdrawal-induced negative affect and reduction in DA

270
Q

acute effects of alcohol on opioid mechanisms

A
  • increases endogenous opioids

- Alcohol self-administration decreased by opioid antagonist or μ opioid receptor knockout

271
Q

chronic effects of alcohol on opioids mechanisms

A

reduces opioid production

272
Q

alcohol treatment: detoxification

A

benzodiazepine replacement

273
Q

alcohol treatment: psychosocial

A

self-help groups

PSYC 336 - Drugs and Behavior (2 decks)

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