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Neuro-pharmacology > Opioids: Reinforcement and Dependence > Flashcards

Opioids: Reinforcement and Dependence Flashcards

1
Q

Reinforcing effects of
opioids Animals readily acquire

A

operant self-administration of
opiates

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2
Q

Self-administration increases over time to a

A

stable/optimal level in blood

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3
Q

Reinforcing effects of
opioids Animals maintain a stable total level

A

separate
pretreatment with morphine will decrease self administration to reach the same approximate levels

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4
Q

Animals readily develop

A

conditioned place preference for
opiate use

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5
Q

Heroin self-administration reaches steady-state levels and are

A

self-regulated by rats. Heroin SA contrasts sharply with
cocaine SA in which use is erratic and subject mortality is
high.

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6
Q

Mesolimbic
dopamine pathway

A

Opioids function within the mesolimbic
dopamine reward pathway

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7
Q

Dopaminergic projections from the
ventral tegmental area (VTA) project to

A

the Nucleus accumbens (NAc) providing
motivational salience to information
passing to the ventral palladium.

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8
Q

In the absence of reinforcing stimuli Dopamine
release is under

A

r tonic inhibitory control of
GABA interneurons.

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9
Q

Dopamine release in the NAc provides a

A

positive reinforcement to associated
behaviours

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10
Q

Opioids function within the

A

mesolimbic dopamine reward
pathway

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11
Q

Mesolimbic
dopamine pathway -Endorphin-secreting neurons
provide

A

inhibitory input to
GABAergic interneurons in the
VTA.

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12
Q

Mesolimbic
dopamine pathway Endorphin release or MOR
activation results in

A

disinhibition
of NAc DA release

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13
Q

Opiates act at

A

GABAergic
interneuron terminals (axoaxonal
transmission) to disinhibit NAc
dopamine release and increase
motivational salience.

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14
Q

Mesolimbic
dopamine pathways Dynorphin provides

A

direct inhibitory
control over the mesolimbic DA
neurons.

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15
Q

Mesolimbic
dopamine pathways Dynorphin release or KOR activation
results in

A

inhibition of NAc DA release.

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16
Q

Reinforcing effects of opioid receptor agonists Agonists at μ and δ receptors are

A

reinforcing and readily lead to self-administration and conditioned place
preference (CPP)

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17
Q

Reinforcing effects of opioid receptor agonists
Agonists at the κ receptor

A

r do not
acquire self-administration and will
actually induce conditioned place
aversion

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18
Q

Reinforcing effects of opioid receptor agonists * Endogenous opioids provide

A

salience
through mesolimbic DA modulation

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19
Q

Endogenous opioids provide salience
through mesolimbic DA modulation Opiates act principally through

A

μ-opioid
receptors to provide incentive salience

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20
Q

Endogenous opioids provide salience
through mesolimbic DA modulation Dynorphins act through

A

κ-opioid
receptors to provide aversive salience

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21
Q

Dopamine lesion using 6-OHDA

A

reduces but does not abolish opiate
self-administration

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22
Q

Reinforcement

A

Opiates and other drugs of abuse are considered to engage natural reward circuitry in a manner
that bypasses the need for sensory input / processing

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23
Q

Relative intensity of reinforcement is thought to relate to the more

A

direct coupling of drug
administration with activation of reward circuitry

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24
Q

Reinforcement increases with

A

different routes of drug administration

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25
Q

Heroin is more reinforcing than

A

morphine due to more rapid transit across the BBB

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26
Q

IV administration is more reinforcing than

A

oral or IM administration due to more rapid access to the BBB

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27
Q

Drugs available by inhalation (esp. nicotine) have very

A

rapid access to the brain and are highly reinforcing

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28
Q
  • In humans reinforcement by drugs of abuse is thought to be
A

far stronger than natural rewardS

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29
Q

Reduced self-care is common among

A

drug users – including poor or insufficient diet

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30
Q

Rebound hyp eractivity

A

As opiates are depressants (in that they depress CNS
function) their withdrawal results in CNS hyperactivity

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31
Q

Withdrawal symptoms can be described as

A

rebound
hyperactivity as neural circuits operate at a disturbed
homeostatic level

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32
Q

Withdrawal effects contrast/oppose

A

acute effects of
intoxication

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33
Q

acute action

A

what the drug does

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34
Q

withdrawal sign

A

opposite of acute action

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35
Q

Acute action Analgesia withdrawal sign

A

Pain and irritability

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36
Q

Acute action Respiratory depression withdrawal sign

A

Panting and yawning

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37
Q

Acute action euphoria withdrawal sign

A

dysphoria and depression

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38
Q

Acute action relaxation and sleep withdrawal sign

A

restlessness and insomnia

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39
Q

Acute action tranquilization withdrawal sign

A

fearfulness and hostility

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40
Q

Acute action decreased blood pressure withdrawal sign

A

increased blood pressure

41
Q

Acute action constipation withdrawal sign

A

Diarrhea

42
Q

Acute action pupil constriction withdrawal sign

A

pupil dilation

43
Q

Acute action hypothermia withdrawal sign

A

hyperthermia

44
Q

Acute action drying of secretions withdrawal sign

A

tearing, runny nose

45
Q

Acute action reduced sex drive withdrawal sign

A

spontaneous ejaculation

46
Q

Acute action flushed and warm skin withdrawal sign

A

chillness and goosebumps

47
Q

parts of the brain and receptors responsible for Analgesia

A

MOR– Cortex, 11
Thalamus, PAG,
Raphe Nucleus
KOR– spinal

48
Q

parts of the brain and receptors responsible for respiration depression

A

Medulla

49
Q

parts of the brain and receptors responsible for euphoria

A

Mesolimbic DA

50
Q

parts of the brain and receptors responsible for relaxation and sleep

A

MOR
KOR

51
Q

parts of the brain and receptors responsible for tranquilization

A

KOR

52
Q

parts of the brain and receptors responsible for decreased blood pressure

A

MOR

53
Q

parts of the brain and receptors responsible for constipation

A

MOR in the GI

54
Q

parts of the brain and receptors responsible for pupil constriction

A

KOR

55
Q

parts of the brain and receptors responsible for hypothermia

A

Medulla

56
Q

parts of the brain and receptors responsible for drying of secretions

A

σ-receptor

57
Q

parts of the brain and receptors responsible for reduced sex drive

A

Hypothalamus

58
Q

parts of the brain and receptors responsible for flushed and warm skin

A

MOR

59
Q

In humans behavioural tolerance contributes
to the decreased effects of

A

opiates

60
Q
  • Tolerance and dependence are
A

reversible
adaptive changes to drug use

61
Q

Learning and memory processes can be
demonstrated to contribute to

A

tolerance in
animal models

62
Q

NMDA receptor antagonists (MK801,
dizocilpine) reduce

A

tolerance to analgesia as
measured by tail
-flick latency

63
Q

Physical dependence model

A

Establishment and maintenance of addictions
manifests from development of dependence

64
Q

Abstinence (withdrawal) results in craving,
leading to

A

relapse

65
Q

Posits addiction is a result of

A

negative
feedback in trying to eliminate unpleasantness
of abstinence

66
Q

Models of drug addiction

A

initial drug use -> repeated drug use -> physical dependence -> attempts at abstinence -> withdrawal symptoms -> relapse then relapse back to attempts at abstinence

67
Q

Limitations of physical dependence model (3)

A

Addiction results from physical dependence
Relapse results from withdrawal
Model fails to account for psychological contributions to relapse and craving

68
Q

Addiction results from physical dependence Some addictive drugs do not

A

demonstrate dependence e.g. cocaine

69
Q

Addiction results from physical dependence Dependence can be demonstrated without

A

addiction - Normal dependence in clinical use of opiates

70
Q

Dependence only explains

A

persistent use, not initial use

71
Q

Relapse results from withdrawal - * Relapse can occur well after

A

detoxification

72
Q

Relapse results from withdrawal - Role of classical conditioning in relapse is not well

A

demonstrated in humans – mostly anecdotal
evidence

73
Q

Positive reinforcement model

A

Drug addiction results from
positive feedback – compulsive
desire to experience drug-related
euphoria

74
Q

Euphoria resulting from initial drug
use serves to

A

reinforce additional
use

75
Q

Limitations of positive reinforcement model

A
  • Craving increases with prolonged use
  • Many users voluntarily stop using drugs that are strongly
    reinforcing
76
Q

Limitations of positive reinforcement model - Craving increases with prolonged use

A

euphoric effects tend to diminish with use due to tolerance

77
Q
  • Many users voluntarily stop using drugs that are strongly
    reinforcing
A

individual differences in susceptibility to addictions is not
explained by the reinforcing effects of drug-induced euphoria

78
Q

Positive reinforcement model steps

A

initial drug use -> positive reinforcement -> repeated drug use -> attempts at abstinence -> compulsive desire to re-experience drug-induced euphoria -> relapse then relapse back to attempts at abstinence

79
Q

Incentive-sensitization model steps

A

initial drug use -> positive reinforcement -> repeated drug use -> sensitization of drug wanting but not drug liking -> attempts at abstinence -> compulsive desired for the drug due to sensitized incentive salience system -> relapse then relapse back to attempts at abstinence

80
Q

Incentive-sensitization model

A

Distinguishes drug liking (drug ‘high’) and drug
wanting (craving)

81
Q

Incentive-sensitization model Increased use occurs with

A

increased wanting even
though drug liking remains the same or decreases

82
Q

Increased use occurs with increased wanting even
though drug liking remains the same or decreases - Proposes two distinct

A

underlying neurobiological
processes for liking and wanting

83
Q

Incentive-sensitization model - Drug wanting system undergoes

A

sensitization - Mesolimbic DA system readily sensitized

84
Q

Incentive-sensitization model Drug liking system undergoes

A

Tolerance

85
Q

Opponent-process model

A

Affective processes responsive to strong
stimuli (e.g. euphoria) are balanced by
opposing affective responses that is
experienced after initial response ends

86
Q

Affective stimuli would be the _____ opponent process would be the ______

A

High - Withdrawal

87
Q
  • Repeat presentation of strong stimuli results in
A

strengthening of the opponent process

88
Q

Adaptive processes lower

A

r hedonic set point
such that chronic users experience dysphoria
in the absence of drugs

89
Q

Limits of incentive-sensitization and opponent process models (Both)

A

Both address neural mechanisms of drug abuse
- Both explain different aspects of addiction

90
Q

Limits of incentive-sensitization and opponent process models (Both) - * Both explain different aspects of addiction

A
  • Incentive-sensitization provides an explanation of drug craving
  • Opponent-process provides an explanation of dysphoria during
    withdrawal
91
Q

Limits of incentive-sensitization and opponent process models (neither)

A

Neither model addresses initial drug use

92
Q

Limits of incentive-sensitization and opponent process models - Limited incorporation of

A

psychosocial factors contributing to
addictive patterns of use

93
Q

Disease models of addiction

A

Propose that drug addiction results
from inherent differences in
susceptibility

94
Q

Propose that drug addiction results
from inherent differences in
susceptibility - Exposure to

A

drug in some individuals
results in loss of control over intake

95
Q

Disease models of addiction -Most widely accepted for

A

alcoholism

96
Q

Disease models of addiction Alternate explanation is that

A

drug
exposure alters brain function leading
to loss of control

97
Q

Disease models of addiction Drug use initiation is

A

necessary but not
sufficient for development of a
substance-use disorder

98
Q

Disinhibition (predisposition to
impulsivity, hyperactivity, antisociality)

A

s a predictive risk of substance-use
(regardless of the substance)

99
Q

Disease model removes the

A

moral
aspects of addictions

Neuro-pharmacology (26 decks)

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