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Behavioral Pharmacology > Chapter 12: Cocaine and Amphetamines > Flashcards

Chapter 12: Cocaine and Amphetamines Flashcards

1
Q

cocaethylene

A

Metabolite formed from the interaction of cocaine and alcohol. It produces biological effects similar to those of cocaine but has a longer half life.

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2
Q

cocaine binges

A

Periods of cocaine use lasting hours or days with little or no sleep.

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3
Q

contingency management program

A

Type of addiction treatment program in which the client’s drug taking is monitored by regular urine testing and abstinence is reinforced with vouchers redeemable locally for consumer products or services.

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4
Q

crack

A

Form of cocaine made by adding baking soda to a solution of cocaine HCl, heating the mixture, and drying the solid.

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5
Q

drug-seeking behavior

A

Performance of an operant response such as a lever-press or a nose-poke with the expectation of receiving delivery of a drug dose.

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6
Q

expression

A

Process that leads to manifestation of a sensitized response and that requires enhanced reactivity of DA nerve terminals in the nucleus accumbens.

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7
Q

focused stereotypies

A

Behaviors produced by high doses of psychostimulants (e.g., cocaine and amphetamine) and characterized by repetitive and aimless movement.

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8
Q

freebasing

A

Smoking the freebase form of cocaine obtained by dissolving cocaine HCl in water, adding an alkaline solution, and then extracting with an organic solvent.

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9
Q

incubation

A

Time-dependent increase in drug craving and drug seeking behavior during abstinence.

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10
Q

induction

A
  1. Increase in liver enzymes specific for drug metabolism in response to repeated drug use. 2. Process that establishes psychostimulant sensitization by activating glutamate NMDA receptors and, in some cases, D1 receptors.
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11
Q

mephedrone

A

Cathinone derivative (4-methylmethcathinone) that is an emerging abused stimulant drug. It is a member of a group of compounds sometimes called “legal highs.”

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12
Q

narcolepsy

A

Sleep disorder characterized by repeated bouts of extreme sleepiness during the daytime. Symptoms include sudden cataplexy, sleep paralysis, and dream-like hallucinations.

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13
Q

psychosocial treatment programs

A

Counseling programs that involve educating the user, promoting behavioral change and alleviating problems caused by drug use.

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14
Q

relapse prevention therapy

A

Treatment program for drug abusers that teaches an individual how to avoid and cope with high-risk situations.

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15
Q

sympathomimetic

A

Substance that produces symptoms of sympathetic nervous system activation.

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16
Q

psychomotor stimulants

A

marked sensorimotor activation; increase alertness, heighten arousal, and cause behavioral excitement

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17
Q

naturally occurring form of cocaine

A

alkaloidal cocaine

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18
Q

two synthetic forms of cocaine

A

WIN 35,428 (CFT) and RTI-55; more potent than cocaine

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19
Q

how cocaine is extracted

A

coca leaves contain between .6% and 1.8% cocaine. Initial extraction of the leaves results in coca paste containing about 80% cocaine. The alkaloid is then converted to hydrochloride (HCl) salt and is crystalized.

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20
Q

two ways cocaine is transformed into cocaine freebase

A
  1. freebasing

2. crack

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21
Q

is smoking crack the same as doing cocaine?

A

the heat in smoking crack produces unique chemical products that can be detected in the urine

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22
Q

how cocaine exerts its effects

A

is lipophilic (fat soluble) and readily passes through the BBB; once absorbed into circulation, it is rapidly broken down by enzymes found in the blood stream and liver

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23
Q

how long do cocaine’s effects last?

A

half life is .5-1.5 hours, but the high only lasts about 30 minutes

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24
Q

benzolecgonine

A

major metabolite in cocaine; can be detected in urine for several days following last dose

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25
Q

mechanisms of action for cocaine

A

blocks the reuptake of three monoamine neurotransmitters (DA, NE, 5-HT); these neurotransmitters are cleared from the synaptic cleft by membrane proteins called transporters. cocaine binds to the transporters to inhibit their function which leads to increased neurotransmitter levels in the synaptic cleft and an increase in transmission at the affected synapses.

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26
Q

what neurotransmitter transporter does cocaine bind most strongly with?

A

5-HT, then DA, then NE

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27
Q

what does the blockage of DA reuptake do?

A

important for cocain’s stimulating, reinforcing, and addictive properties

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28
Q

what does cocaine do at high concentrations?

A

also inhibits voltage-gated sodium (Na+) channels in nerve cell axons which causes a block in nerve cell conduction. Thus it can be used as a local anesthetic by preventing transmission of nerve signals along sensory nerves

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29
Q

behavioral effects of cocaine

A

high, feelings of exhilaration and euphoria, sense of well-being, alertness, heightened energy, diminished fatigue, self-confidence, a rush, increases sociability and talkativeness, heightened sexual interest, increase in aggressive behavior, increased behavioral activation

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30
Q

physiological consequences of cocaine

A

increased heart rate, vasoconstriction, hypertension (increased blood pressure), hyperthermia (elevated body temperature), seizures, heart failure, stroke, intracranial hemorrhage

31
Q

what happens if you create a neurotoxic lesion in the nucleus accumbens?

A

prevents psychostimulant induced locomotion

32
Q

what happens if you create a neurotoxic lesion in the striatum?

A

antagonize the stereotypes associated with higher drug doses

33
Q

what does the mesolimibic DA to the nucleus accumbens play a role in?

A

the reinforcing effects

34
Q

mutant mice lacking DA transporter DAT

A

fail to show hyperactivity following psychostimulant use

35
Q

drug seeking behavior

A

performance of an operant response such as a lever-press or a nose-poke with the expectation of receiving delivery of a drug dose

36
Q

what does the nucleus accumbens also seem to play a role in?

A

the urge to take cocaine in dependent users who are attempting to maintain abstinence

37
Q

what causes the high?

A
  1. the drug binds to DAT and prevents DA reuptake; once a certain level of DAT occupancy (40-60%) is attained following cocaine or methyphenidate administration, the subject may experience a high; injection/smoking quickly blocks DAT and thus creates a high
  2. baseline level of DA activity in the mesolimbic pathway
38
Q

DA receptors types

A

D1-D5; D1 and D5 are the D1-like family; D2, D3, D4 are the D2-like family

39
Q

D1 receptors

A

locomotor-stimulating effects; D1 knockout mice do not self-administer

40
Q

D2 receptors

A

mice lacking D2 self-administer cocaine

41
Q

D3

A

present in the mesolimbic DA areas such as the nucleus accumbens; rewarding and reinforcing effects

42
Q

what protects against long-term abuse of cocaine?

A

a strong anxiety response, unavailability of the drug, the cost, social and legal consequences, fear of losing control,

43
Q

what percentage of users abuse it?

A

10-15% of initial intranasal users eventually become abusers

44
Q

abstinence syndrome following a cocaine binge

A

crash; depressed mood; exhaustion; anhedonia, lack of energy, anxiety, craving,

45
Q

brain abnormalities in cocaine dependent users?

A

abnormal prefrontal cortical functioning that is manifested as deficits in inhibitory control and in monitoring and evaluating consequences of their behavior

46
Q

brain activity when presented with drug related stimuli

A

DA release in dorsal striatum (caudate and putamen); the midbrain-striatal DA pathway is part of a larger circuit that is activated when cocaine users experience craving

47
Q

transition to compulsive use

A

longer periods of access to cocaine can lead to an escalation of intake that down-regulates the reward circuit. This presumably makes the cocaine less rewarding and thus supports further increases in drug consumption

48
Q

what is addiction a result of?

A

a combination of prolonged exposure to the drug, which can be seen from the fact that changes in behavior occurred only after many self-administration sessions and factors that lead to differential vulnerability among individuals

49
Q

sensitization phases

A
  1. induction
  2. expression
    during the period between these two phases sensitization can actually increase in strength as the result of ongoing neurochemical changes in the brain
50
Q

what tends to show tolerance over time?

A

cocaine’s euphoric effects

51
Q

neural mechanisms of sensitization

A

DA activity in the VTA plays an important role in locomotor sensitization; medial prefrontal cortex which sends a glutamatergic projection to the VTA and the NaCC

52
Q

neural mechanisms of tolerance

A

baseline level of D2 receptor binding is reduce in cocaine-dependent subjects; the DA system is less responsive to DA reuptake blockade which contributes to behavioral tolerance

53
Q

problems associated with repeated cocaine use?

A

stroke or seizure, abnormalities in gray and white matter in cerebral cortex, decreased volume of some cortical regions and striatum, impairment in cognitive functions, including verbal memory, attention and motor function, chest pains, irregular heart rate, damaged heart muscle, heart attack, perforation of the nasal septum, panic attacks, paranoid psychosis with delusions and hallucinations

54
Q

using antabuse (disulfiram) for the treatment of cocaine abuse

A

inhibits the enzyme aldehyde dehydrogenase and inhibits dopamine beta-hydrozylase (DBH) the enzyme that synthesizes NE from DA and inhibits esterases that are involved in the breakdown of cocaine

55
Q

cocaine vaccine

A

antibodies bind to cocaine molecules or may have catalytic activity that actually breaks down cocaine in the bloodstream

56
Q

amphetamines

A

synthetic psychostimulants available in two forms, L-amphetamine and D-amphetamine

57
Q

how to take amphetamines?

A

typically either orally, IV, or subcutaneous injection; takes up to 30 minutes for behavioral effects after a typical oral dose of 5-15 mg

58
Q

is methamphetamine the same?

A

it is a more potent form

59
Q

speedball

A

to moderate the extreme stimulatory effect of IV amphetamine or meth by combining it with heroin

60
Q

how are amphetamines/ meth metabolized?

A

in the liver and excreted in the urine; half life ranges from 7 to 30 hours for amphetamine and 10 hours for meth

61
Q

mechanisms of action of meth and amphetamine

A

are indirect agonists of the catecholaminergic systems and release catecholamines from nerve terminals. at very high doses they inhibit catecholamine metabolism by monoamine oxidase;

62
Q

catecholamine release in amphetamines/ meth

A
  • cause DA molecules to be released from inside the vesicles into the cyctoplasm of the nerve terminal; then DA molecules are transported outside the terminal by a reversal of the DAT, the result is a massive increase in synaptic DA concentrations and an association stimulation of DA transmission; DAT reversal is facilitated by an activation of protein kinase C and calcium/ calmodulin kinase II resulting in phosphorylation of the transporter
  • NE releasing effects of amphetamines occur in the brain and the sympathetic nervous system
63
Q

behavioral effects of amphetamine

A

heightened alertness, increased confidence, feelings of exhilaration, reduced fatigue, generalized sense of well-being, improved performance on simple, repetitive psychomotor tasks, delay in sleep onset, reduction in REM, enhanced athletic performance, psychotic reactions, neurotoxicity

64
Q

uses of amphetamine

A

narcolepsy, ADHD, suppression of appetite and weight reduction (antiobesity treatment);

65
Q

withdrawal of amphetamine

A

depressed mood, increased anxiety, sleep disturbances, cognitive deficits, craving, agitated behavior, reduced energy, increased appetite; may take up to several weeks to subside

66
Q

are men more likely to become dependent on meth?

A

no

67
Q

Psychotic reactions to amphetamine

A

visual/auditory hallucinations, behavioral disorganization, paranoid state with delusions of persecution, parasitic skin infestation; occurs only after a chronic abuse pattern

68
Q

risk factors for psychotic reactions

A

long history of use, high doses, dependence, a preexisting history of psychotic symptoms

69
Q

neurotoxicity

A

long lasting reductions in levels of DA, tyrosine hydrozylase (enzyme in DA synthesis), DAT in the striatum, damage to DA axons and terminals, damage to serotenergic fibers in the neucortex, hippocampus, and striatum

70
Q

what likely causes neurotoxicity?

A

oxidative stress (cellular stress due to increased production of oxygen containing free radicals), excitotoxicity, neuroinflamation, and mitochondrial dysfunction

71
Q

loss of striatal DA

A

could potentially predispose heavy users to an early onset of Parkinson’s disease

72
Q

physical health and amphetamine use

A

cardiovascular problems, elevated heart rate and blood pressure, atherosclerosis, myocardial infarction, increased risk of stroke, increased mortality rate, premature aging

73
Q

info about mephedrone

A

snorted, causes euphoria and energy, inhibits 5-HT and DA uptake and increases extracellular levels of both in the NaCC, sympathomimetic toxicity, agitation, seizures, death; DA and 5-HT toxicity

Behavioral Pharmacology (11 decks)

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