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Behavioral Pharmacology > Ch 9: Addiction > Flashcards

Ch 9: Addiction Flashcards

1
Q

abstinence syndrome

A

Condition characterized by unpleasant symptoms when an individual tries to cease drug use.

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2
Q

allele

A

Alternative form of a gene. Multiple alleles of a gene differ by one or more nucleotides in the gene’s DNA sequence and may code for proteins with slightly different amino acid sequences.

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3
Q

allostasis

A

Adaptive biological process in which an organism’s response to repeated threats or challenges results in long-lasting physiological or behavioral changes. This concept is distinguished from homeostasis, which refers to the tendency of an organism to maintain physiological or behavioral stability in the face of threats or challenges (i.e., to remain unchanged).

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4
Q

anhedonia

A

Difficulty or lack of the ability to experience pleasure. Such a state is characteristic of many depressed patients and may also occur during drug withdrawal in an addicted person.

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5
Q

anti-reward system

A

Neural system that is thought to be engaged during the transition from impulsive to compulsive drug use. This system is an important contributor to the negative mood state induced by withdrawal from abused drugs.

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6
Q

biopsychosocial model

A

Model of addiction that attempts to give a full account of addiction by incorporating biological, psychological, and sociological factors.

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7
Q

breaking point

A

The point at which an animal will no longer expend the effort required to receive the reward (e.g., in a drug self-administration paradigm).

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8
Q

comorbidity

A

Diagnosis of simultaneous but distinct disease processes in an individual, such as the propensity for drug abusers to be diagnosed with other psychiatric problems.

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9
Q

craving

A

Strong urge addicts feel, compelling them to take a drug.

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10
Q

Delta FosB

A

Member of the Fos family of transcription factors. This protein accumulates in some brain areas (nucleus accumbens, dorsal striatum) after repeated exposure to various drugs of abuse and is hypothesized to contribute to the development of an addicted state. accumulation of this lasts at least several weeks after last drug administration bc the protein has a long half-life

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11
Q

disease model

A

Model of addiction that treats addiction as a distinct medical disorder or disease; based largely on evidence of dysregulation of brain function in addiction and on the idea that such dysfunction is at least partly caused by repeated drug exposure (neuroadaptations)

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12
Q

drug detoxification

A

Process whereby an individual eliminates a drug from the body and goes through an abstinence syndrome.

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13
Q

drug priming

A

Delivery of a small dose of a drug by the experimenter for the purpose of eliciting drug-seeking behavior, typically in an animal whose drug self-administration responding was previously extinguished.

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14
Q

drug reward

A

A positively-motivating subjective response to a drug, often experienced by humans as a euphoric feeling or “high.”

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15
Q

electrical self-stimulation

A

A procedure whereby an animal self-administers a weak electrical shock to a specific brain area due to the reinforcing properties of the stimulation.

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16
Q

executive function

A

Collection of higher-order cognitive abilities including planning, organization, problem solving, mental flexibility, and valuation of incentives. The prefrontal cortex plays an important role in executive function.

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17
Q

Gateway Theory

A

Theory proposing that use of certain drugs of abuse, particularly during childhood or adolescence, increases the risk of progressing to other substances. For example, tobacco or alcohol have been proposed as gateways to marijuana use, and in turn marijuana has been proposed as a gateway to so-called “hard drugs” like cocaine or heroin.

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18
Q

Heritability

A

The relative contribution of genetics to the variability of a trait within a population; .3-.8 for substance use disorders

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19
Q

Impaired response inhibition and salience attribution (IRISA)

A

Theory of addiction that emphasizes prefrontal cortical deficits leading to difficulty in refraining from drug use (impaired response inhibition) and the development of an abnormal psychological state in which drugs have much greater motivational power than normal reinforcers (impaired salience attribution).

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20
Q

moral model

A

Model of addiction that treats addiction as a personal and moral problem; reason why the medical model exists (to reduce sense of guilt)

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21
Q

natural recovery

A

Recovery from drug addiction without the aid of treatment; generally have less severe substance use problems

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22
Q

neuroadaptation

A

Changes in brain functioning that attempt to compensate for the effects of repeated substance use.

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23
Q

opponent-process model

A

Model of addiction in which the initial positive response to a drug is followed by an opposing withdrawal response as the drug wears off; over time repeated presentations of the stimulus altered the opponent process by strengthening its magnitude, reducing its latency to onet, and increasing its duration

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24
Q

place conditioning

A

Pavlovian conditioning procedure used to test the rewarding effects of drugs in rats and mice; the animals are exposed to drugs in specific compartments of an apparatus–with animals later choosing to spend more time in the drug compartment later on

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25
Q

positive reinforcer

A

Something (e.g., an abused drug) that, when provided to an organism, increases the strength of the response that was used to obtain the item. In studies of addiction, the positive reinforcing quality of a drug is usually measured by means of a self-administration procedure.

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26
Q

progressive-ratio procedure

A

Method used to measure the relative power of drug reinforcement by steadily increasing the response to reward ratio. Eventually leads to the breakpoint

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27
Q

relapse

A

Recurrence of drug use following a period of abstinence.

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28
Q

remission

A

Period in which an addict is drug free.

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29
Q

reward circuit

A

Circuit of neurons that, when activated, mediates the rewarding effects of both natural rewards (e.g., food, water, sex) and drugs of abuse.

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30
Q

schedule of controlled substances

A

System established by the Controlled Substances Act in 1970 that classifies most substances with abuse potential into one of five schedules. Schedules I and II have the strictest guidelines.

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31
Q

self-medication hypothesis

A

Theory that addiction is based on an effort by the individual to treat oneself for mood or other ill feelings.

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32
Q

shared etiology

A

Situation in which multiple disorders are caused by the same set of factors. thus similiar things may lead to both addiction AND other psychiatric illness

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33
Q

substance abuse

A

Disorder involving the overuse of a drug by an individual. It may or may not lead to substance dependence.

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34
Q

substance dependence

A

Disorder involving excessive and harmful drug use by an individual, corresponding to addiction.

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35
Q

substance use disorder

A

New DSM-5 designation for a psychiatric disorder with features typically associated with addiction. This designation replaces both substance abuse and substance dependence categories in DSM-IV. A maladaptive pattern of substance use, over at least a 12 month period, that has led to significan impairment or distress by clinical standards

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36
Q

how many people are currently users of drugs?

A

22.5 million

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37
Q

Pure food and drug act

A

1906 regulated labeling of patent medicines and created the FDA

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38
Q

Harrison Act

A

1914 regulated the dispending and use of opioid drugs and cocaine

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39
Q

Eighteenth Constitutional Amendment

A

1920 prohibition; banned alcohol sales except for medicinal use

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40
Q

marijuana tax act

A

1937 banned nonmedical use of cannabis

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41
Q

controlled substances act

A

1970 established the schedule of controlled substances and created the DEA

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42
Q

physical dependence

A

abstinence from the drug leads to highly unpleasant withdrawal symptoms that motivate the individual to reinstate drug use

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43
Q

Definition of addiction

A

a behavioral pattern of drug use, characterized by overwhelming involvement with the use of a drug (compulsive use), the securing of its supply, and a high tendency to relapse after withdrawal

44
Q

8 behaviors that are similiar to drug use

A

gambling, eating disorders, excessive internet use, preoccupation with love, preoccupation with sex excessive and compulsive exercising, workaholism, and compulsive shopping/spending

45
Q

behavioral addictions

A

failure to resist an impulse, drive, or temptation to perform an act that is harmful to the person or to others

46
Q

Two types of drug progression

A
  1. Gateway theory
  2. changes in the amount, pattern, and consequences of drug use as they affect the user’s health and functioning. May or may not progress to nonproblematic use
47
Q

3 components of pathological drug use as a cyclical pattern

A
  1. periods of preoccupaiton with drugs and anticipation up upcoming use
  2. periods of drug intoxication that in some cases are associated with binging on the drug
  3. periods following drug use that are characterized by withdrawal symptoms and negative affect
48
Q

maturing out

A

alcohol and marijuana use tend to naturally decrease as individuls enter adulthood and begin to take on adult responsibilities

49
Q

schedule I substances

A

substances that have no accepted medical use and have a high abuse potential (heroin, LSD, mescaline, marijuana, MDMA)

50
Q

Schedule II substances

A

substances that have a high abuse potential with severe psychotic or physical dependence liability (opium, morphine, codeine, amphetamine, ritalin, PCP)

51
Q

schedule III substances

A

substances that have an abuse potential less than those in schedules I and II, including compounds containing limited quantities of certain narcotics and nonnarcotic drugs (barbiturates other than those in another schedule, paregoric)

52
Q

Schedule IV drugs

A

substances that have an abuse potential less than those in schedule III (phenobarbital, valium, xanax)

53
Q

schedule V drugs

A

substances that have an abuse potential less than those in schedule IV, consisting of preparations containing limited amounts of certain narcotic drugs generally for antitussive (cough suppressant) and antidiarrheal purposes

54
Q

how do rates of administration relate to addiction?

A

routes that cause the fasted onset of drug action having the greatest addiction potential because they produce the strongest euhoric effects; However, fast onset is associated with a shorter duration of action

55
Q

IV drug self-administration

A

substances that are strong reinforcers in the self-IV paradigm always have a great abuse liability in humans when taken intravenously or by smoking;

56
Q

ways to effectively model relapse

A
  1. the experimenter delivering a small dose of the drug to the animal (drug priming)
  2. subjecting the animal to stress
  3. exposing the animal to environmental cues that were previously paired with drug delivery (prior to extinction)
57
Q

why dont the negative consequences of addiction counteract the positive reinforcement?

A

possibly because drug induced euphoria occurs very quickly and the negative consequences occur later in time

58
Q

can rewarding drugs be averisve?

A

YES! some substances can be reinforcing when self-administered by aversive when administered by an experimenter

59
Q

physical dependence and continued drug use

A

some drugs lead to physical dependence, which causes unpleasant withdrawal symptoms when stopped. this can lead the user to take the drug again (relapse) to alleviate symptoms (negative reinforcement)

60
Q

progression of drug taking behavior

A

impusive stage: primary motivation is the positive reinforcing effects

compulsive stage: primary motivation is the negative reinforcement of relief from withdrawal

61
Q

what is a crucial symptom associated with conditioned withdrawal?

A

drug craving

62
Q

what areas of the brain are activated by procuremen and use of evoked craving?

A

Increased: amygdala; anterior cingulate cortex

decreased: basal ganglia

63
Q

what does drug seeking for relief from withdrawal fail to explain?

A

individuals who have gone through detox

64
Q

factors that contribue to relapse

A

exposure to drug related stimuli, stress, boredom, lack of other reinforcers, desire to get high

65
Q

internal states as cues

A

drugs can produce internal states that can serve as cues controlling the animal’s behavior in a learning task–> experienced users come to expect these subjective effects, and these expectations are thought to contribute to the persistence of drug-seeking/using behaviors

66
Q

how many genes have been found to be addiction related?

A

1500

67
Q

is genetic involvement of addiciton similiar across substances?

A

there is evidence for a common genetic involvement of 5 different molecular pathways across addictions to alcohol, nicotine, cocaine, opiate drugs

68
Q

risk factors for abuse

A

younger age, less education, nonwhite ethnicity, lack of employment, stress and the person’s ability to cope with stress

69
Q

what are addicts also typically diagnosed with?

A

anxiety, mood or personality disorders

70
Q

three personality related pathways to addiction

A
  1. behavioral disinhibition: deviant behaviors (abuse) are linked to a trait cluster of impulsivity, antisociality, unconventionality, agressiveness, low levels of constraint and harm avoidance
  2. stress reduction: stress reactivity, anxiety, neuoticism–> vulnerability to stress
  3. reward sensitivity: sensation seeking, reward seeking, extraversion, gregariousness
71
Q

Does it matter if your parent is an alcoholic?

A

children are at an increased risk for having alcohol or other substance abuse problems; may be related to modeling of the parent’s drinking behavior or to a heightened expectancy that drinking will lead to positive mood changes

72
Q

4 functions served by drug abuse

A
  1. social facilitation
  2. remove the user from normal social roles and responsibilities
  3. promote group solidarity within a particular ethnic group
  4. drug subculture that embraces social rituals surrounding a particular subculture
73
Q

what can reduce the risk of relapse?

A

moving to a new area, devloping new social relationships, obtaining employment, engaging in sbustitute activities like exercise or meditation

74
Q

pathways in the reward circuit

A

mesolimbic and meocortical dopamine pathways; bed nucleus of the stria terminals; medial forebrain bundle; output pathway from the NAcc to the ventral pallidum

75
Q

medial forebrain bundle

A

a collection of ascending and descending fibers that connects that ventral tegmental area with areas of the ventral forebrain including the nucleus accumbens, septal area, and olfactory tubercle

76
Q

mesolimbic and meocortical dopamine pathways

A

that originate in the ventral tegmental area (VTA) of the midbrain and terminate in the nucleus accumbens (NAcc), amygdala (AMG), and frontal cortex (FC);

77
Q

how do psychostimulants (cocaine/ amphetamine) exert their rewarding effects?

A

increasing transmission at the dopaminergic terminals in the nucleus accumbens.

78
Q

how do opioid drugs and endogenous opioid peptides activate the reward circuit?

A

by stimulating opioid receptors in the ventral tegmental area, nucleus accumbens, amygdala

79
Q

how does alcohol exert its effect?

A

enhances action of y-aminobutric acid (GABA) on GABAa receptors and this enhances DA release in the nucleus accumbens and opioid peptide release in the ventral tegmental area, nucleus accumbens, and the amygdala

80
Q

what does nicotine activate?

A

the reward circuit by stimulating the nicotinic cholinergic receptors in the ventral tegmental area, nucleus accumbens, and amygdala; increases DA release

81
Q

what does THC activate?

A

endogenous cannabinoids and THC stimulate cannabinoid receptors in the same brain areas; increase DA release

82
Q

what plays a role in drug reward?

A

the mesolimbic DA pathway; the DA system is essential for drug reward only for some substances (cocaine/amphetamine) and not for others (heroine/ alcohol); opioid and cannabinoid systems are also involved

83
Q

3 components of reward

A
  1. emotion/affect: subjective feelings of pleasure
  2. motivation: desire to obtain incentives
  3. learning/cognition: expectation that a particular action will lead to attainment of an incentive and strengthening of specific stimulus-response associations based on deliverty of the incentive
84
Q

two types of neuroadaptations

A
  1. within-system
  2. between-system
85
Q

within-system neuroadaptation

A

take place within the reward circuit and constitute a progressive down-regulation of activity in this circuit–> type of tolerance whereby the user experiences less pleasure from each episode of drug use

86
Q

between system neuroadaptations

A

gradual recruitment of a neural circuit (anti-reward system) which leads to increased release of NE and two neuropeptides (corticotropin-releasing factor and dynorphin). This system puts a limit or brake on rewardand it mediates some of the averise effects of stress; plays a major role in the averise effects of withdrawal

87
Q

brain changes after drug use that lead to addiction

A

transition from the nucleus accumbens to the dorsal striatum (caudate putament) as a key area for drug taking behavior–> this area is implicated in stimulus response habit learning which plays a significant role in the progression of drug taking from a reward-moticated behavior to a behavior that is automatic, habitual, and compulsive.

Disruptions of the glutamatergic pathway from the PFC to the nucleus accumbents–> impair the ability of the PFC to mediate response inhibition and impulse control

88
Q

can drugs alter genes?

A

yes they can effect gene expression and proteins

89
Q

transcription factors

A

proteins located in the cell nucleus that either stimulate or inhibit expression of a target gene (the rate of mRNA transcription) and accordingly up or down regulate levels of the protein encoded by the gene.

90
Q

delta FosB overexpressing animals

A

show enhanced sensitivity to a variety of drug effects with the exception of morphine induced analegia

91
Q

does delta FosB alter the brain?

A

yes–proteins regulated by delta FosB are involved in glutamate transmission and structural plasticity within the nuculeus accumbens

92
Q

what may delta FosB play a major role in?

A

transition from controlled drug use to addiction

93
Q

what does delta FosB do?

A

modulates gene and protein expression through epigenetic mechanisms

94
Q

epigenetics

A

chromatin modifications that alter gene expression without changing the nucleotide sequence of the DNA strand

95
Q

two types of epigenetic modifications

A
  1. methylation of the DNA at specific cytosines in the promoter region of the gene; promotes compaction of the chromatin (repressing gene expression)
  2. various modifications of the histone proteins that form complexes around which the DNA double helix is wrapped; facilitates gene expression by opening the chromatin and allowing transcriptional machinery to bing to DNA
96
Q

most studied histone modification

A

acetylation–attachment of acetyl groups to specific sites along the tail of the protein

97
Q

structural brain changes in addiction

A

in the prefrontal cortex (motivation; emotion regulation); executive function; reduced gray matter; volume reductions in the DLPFC, anterior cingulate cortex, orbitofrontal cortex; DA d2 receptor binding in the striatum is correlated with PFC glucose metabolism

98
Q

three major PFC projections

A
  1. dorsolateral circuit that projects from the dorsolateral PFC to the dorsolateral caudate nucleus (executive function)
  2. ventromedial circuit–> connects anterior cingulate cortex with the nucleus accumbens (drive/motivation)
  3. orbitofrontal circuit–> orbitofrontal cortex to the ventromedial caudate (behavioral inhibition/ impulse control)
99
Q

what is the amount of structual damage related to?

A

the severity / longevity of drug use

100
Q

role of the striatum

A

cortical striatal loop: input from the midbrain DA neurons act on striatal D1 and D2 receptors to modulate striatal outflow and activity in the cortical striatal loops. Reduced D2 receptor levels may cause functional deficits (poor impulse control/ planning/ emotion regulation, abnormal salience attribution)

101
Q

role of PFC and drug withdrawal

A

the ability of the dorsal PFC to exert behavioral control is diminished–> lead to a conflict over drug-taking behavior and increased vulnerability to taking more drugs. during repeated drug taking/ intoxication the “hot” drug related functions of the ventral PFC act to suppress the “cold” non-drug related activity of the dorsal PFC and cause the addict to engage overwhelmingly in attending to, seeking out and taking drugs without restraint

102
Q

reward syste

A

mediates the acute rewarding and reinforcing effects of abused drugs–> important for initial stages of drug use and abuse

103
Q

addiction and guilt

A

most individuals will likely have one or more lapses–danger is that guilt and diminished self-worth will engender hopelessness and lead to loss of control and a full blown relapse back to compulsive use.

104
Q

disease

A

a pathological condition of the body that presents a group of clinical signs and symptoms and laboratory findings peculiar to it and that sets the condition apart as an abnormal entity differing from other normal or pathological body states

105
Q

criticisms of disease model

A
  • don’t know if same neuronal changes underly all drug addiction
  • others view it as a behavior pattern that comes about as the result of interaction between many factors (environment, behavioral modeling, positive reinforcing effects of abuse drugs, the reinforcing consequences of avoiding or eliminating drug withdrawal and conditioning to drug related stimuli)

Behavioral Pharmacology (11 decks)

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