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Neuro-pharmacology > cocaine > Flashcards

cocaine Flashcards

1
Q

Stimulants

A

Psychoactive drugs producing a
temporary increase in mental function

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2
Q

Psychostimulants

A

Alertness, wakefulness, and
locomotion

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3
Q

Psychomotor stimulants

A

Cocaine, amphetamines, caffeine,
nicotine

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4
Q

Cocaine Primary psychoactive component has
moderate bioavailability by

A

oral
administration

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5
Q

Cocaine is sensitive to

A

acid hydrolysis

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6
Q

Coca leaves traditionally chewed with lime
to

A

decrease acid hydrolysis in the GI

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7
Q

cocaine administered via

A

oral, IV, or intranasal routes

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8
Q

cocaine is Susceptible to breakdown by

A

heating

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9
Q

cocaine Can be precipitated by heating with

A

baking soda - crack cocaine

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10
Q

Freebase and crack cocaine delivered by

A

inhalation

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11
Q

Cocaine is purified by

A

acid-base
extraction

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12
Q

Illicit cocaine is purified by

A

partially
drying leaves

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13
Q

Inhalation (smoking) or intranasal (snorting)
result in

A

in rapid access to the CNS

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14
Q

Half-life in circulation

A

30-90 minutes.

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15
Q

cocaine Metabolized by

A

esterases, CYP450 in liver

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16
Q

Cocaethylene is an

A

active metabolite formed in the presence of alcohol – longer lasting than cocaine and greater cardiotoxic effects.

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17
Q

Methylecgonidine

A

produced by heating of cocaine and is detectable in urine

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18
Q

Cocaine is amphipathic – meaning it has

A

both hydrophilic and lipophilic nature

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19
Q

Cocaine is amphipathic Subsequently cocaine is very rapidly absorbed

A

across the BBB and measurement of cocaine in circulation does not effectively convey the psychoactive levels

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20
Q

Inhalation and intranasal admin both result in

A

rapid uptake into brain and pronounced psychoactive effects

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21
Q

Rapid uptake into brain and short duration of ‘high

A

(5-30 minutes) thought to contribute to addictive potential

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22
Q

Effects of cocaine “positive” (7)

A

Euphoria
Increased alertness
Increased self-confidence
Increased sociability
Heightened sexual interest / performance
Motor stereotypies
Anorexia

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23
Q

Effects of cocaine “negative” (9)

A

Dysphoria
Irritability, hostility, anxiety
Psychosis
Impulsivity
Increased heart rate
Increased blood pressure
Hyperthermia
Seizures
Stroke / Intracranial haemorrhage

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24
Q

Psychomotor stimulation (7)

A

locomotor
hyperactivity
head bobbing,
pacing,
repetitive rearing,
excess grooming.
compulsive activities such as obsessive cleaning, sorting, organizing

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25
Q

Animal models

A

Animal models will rapidly acquire self-administration of cocaine

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26
Q

Cocaine administration causes

A

hyperactivity in rodents – simple measurement of intoxication

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27
Q

Animals will self-administer to the
point of

A

personal neglect, anorexia, and increased mortality

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28
Q

Cocaine is an

A

SNDRI

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29
Q

SNDRI

A

serotonin, norepinephrine, and dopamine reuptake inhibitor)

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30
Q

Cocaine blocks neurotransmitter reuptake such as at the

A

dopamine transporter (DAT).

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31
Q

Cocaine blocks neurotransmitter reuptake such as at the
dopamine transporter (DAT) This leads to accumulation of

A

neurotransmitters in the synapse and excessive downstream signalling.

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32
Q

At elevated doses cocaine blocks (N)

A

Na+ channels and can be used as a topical anaesthetic

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33
Q

Cocaine Also causes decrease in

A

monoamine synthesis through presynaptic autoreceptors.

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34
Q

Tolerance

A

Cocaine tolerance develops acutely and transiently

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35
Q

Subjective and cardiovascular effects develop tolerance

A

quickly

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36
Q
  • Intermittent use produces
A

sensitization rather than tolerance

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37
Q

In animal models Continuous infusion via minipump results in

A

tolerance to the effects of cocaine

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38
Q

Daily use (intermittent) sensitizes the

A

psychomotor and reinforcing effects

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39
Q

Both animals and humans show

A

cross-sensitization to other stimulants (esp. amphetamines)

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40
Q

Withdrawal

A

No medically serious withdrawal syndrome develops with cocaine use

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41
Q
  • Three phases observed in binge users of cocaine
A
  1. Crash (15-30 minutes following final dose)
  2. Withdrawal (hours-days after final dose)
  3. Extinction
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42
Q

Binge use refers to

A

episodic use for extended periods (hours or days) without interruption (or sleep)

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43
Q

Cocaine crash (7)

A

Dysphoria
agitation
anxiety
depression
strong craving
fatigue after brief period
Exhaustion results in hypersomnolence (prolonged sleep)
Sleep can be interrupted by brief periods of waking and hyperphagia

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44
Q

Withdrawal and Extinction

A

Withdrawal is a period of relatively normal function
Extinction is a gradual return to normal function

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45
Q

Withdrawal is a period of relatively normal function

A

Hours or days of normal mood, sleep, little anxiety
* Little craving for cocaine
* Some report mild cognitive impairment
* Gradual onset of a dysphoric syndrome

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46
Q

dysphoric syndrome (5)

A

boredom, anergia, anhedonia, anxiety, and increased craving

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47
Q

Extinction is a gradual return to normal function

A

Normal mood, normal hedonic function
* Intermittent cravings may occur – particularly in response to emotional or environmental
cues

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48
Q

Toxicity Acute overdose results from several main effects

A

Reduced seizure threshold
Cardiovascular effects
Hyperthermia

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49
Q

Reduced seizure threshold

A

Due to general increase in neurotransmitter release

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50
Q

Cardiovascular effects

A
  • Increased heart rate and blood pressure can increase risk of stroke, cerebral hemorrhage, tachycardia
    and arrhythmia
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51
Q
  • Treatment of overdose is administration of
A

sedative (typically a benzodiazepine) to decrease heart rate and BP, and use of ice or cooling blankets for hyperthermia

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52
Q

Cocaine is the

A

second most popular illicit drug in the USA second to cannabis

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53
Q

(PCE)

A

Prenatal cocaine exposure`

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54
Q
  • In utero exposure to crack-cocaine was
    correlated (in early studies, mostly case studies
    or small cohorts) with
A
  • Premature birth
  • Lower birth weight
  • Mental and physical defects
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55
Q

Public opinion formed around the risks of
PCE leading to prosecution of

A

mothers who
tested positive for cocaine or metabolites

56
Q

Experts predicted a ‘biological underclass’ of delinquents affected by PCE

A

Crime rates were predicted to rise
* Children were predicted to be a burden on school and health care systems

57
Q

Crack cocaine can be explicitly tested by the presence of

A

methylecgonidine

58
Q

Effects of PCE

A

Cocaine readily crosses the placental barrier

59
Q

Animal studies do not support long-term effects of

60
Q

animal studies and cocaine Studies support moderate decreases in

A

learning in the presence of distractions

61
Q

Most described effects of PCE in humans can be attributed to confounding factors

A

Prenatal nutrition
pre- and post-natal care
additional drug use environmental
risks
increased rates of STI

62
Q

Most described effects of PCE in humans can be attributed to confounding factors - Child more likely to be exposed to

A

maternal depression, domestic violence, ‘deadbeat’ parenting – all
affect early childhood development

63
Q
  • Most described effects of PCE in humans can be attributed to confounding factors - Small increased risk of
A

ADHD or increased impulsivity/distractibility

64
Q

Cocaine is

A

sympathomimetic

65
Q

Cocaine elevates NE signalling at

A

noradrenergic
locations

66
Q

Cocaine exerts activating effects on the

A

sympathetic nervous system

67
Q

Cocaine exerts activating effects on the
sympathetic nervous system - Increased

A

heart rate, vasoconstriction,
hypertension, hyperthermia

68
Q

Many adverse effects of cocaine are due to

A

sympathetic activation (stroke, heart failure,
seizure, intracranial hemorrhage)

69
Q
  • Central noradrenergic effects contribute to the
A

psychostimulant effects of cocaine

70
Q

Dopaminergic effects ad cocaine

A

Dopamine plays a central role in the
psychostimulant response to cocaine

71
Q

Dopaminergic effects Two key pathways

A

Nigrostriatal
Mesolimbic

72
Q

Nigrostriatal pathway

A

substantia nigra to the
striatum

73
Q

Mesolimbic pathway

A

ventral tegmentum to
nucleus accumbens

74
Q

Behavioural effects in rodents can be
examined using

A

microinjection and
lesions

75
Q

Microinjection of cocaine into striatum
elicits (Substantia nigra - striatum)

A

stereotyped behaviours

76
Q

Lesion with 6-OHDA antagonizes (substantia nigra - striatum)

A

psychostimulant-induced stereotypies

77
Q

Microinjection of cocaine into NAc elicits (ventral tegmentum to
nucleus accumbens)

A

hyperactivity

78
Q

(ventral tegmentum to
nucleus accumbens)
* Lesion with 6-OHDA blunts

A

psychostimulant-induced hyperactivity

79
Q

lesion of the mesolimbic system

A

diminishes reinforcing effects of
cocaine administration

80
Q

Basal ganglia and affects of dopamine of the direct and indirect pathways

A

Dopamine balances activity between the
direct and indirect pathways

81
Q

Activation of nigrostriatal dopamine
pathways promotes the

A

direct pathway (D1 – excitatory) over the indirect
pathway (D2 – inhibitory).

82
Q

Cocaine elevates DA in the striatum and

A

drives locomotor activity (often
purposeless).

83
Q

Euphoric and
reinforcing
effects

A

Euphoric effects (subjective ‘high’) has been well
studied by PET imaging

84
Q

cocaine occupies what transporter

A

DAT occupancy by cocaine

85
Q

D2R occupancy by

86
Q

Rate of onset of DAT occupancy correlates with

A

intensity of euphoria

87
Q

level of intensity depending on intake

A

Smoking > IV > Intranasal > Oral

88
Q

Individuals with increased D2 receptor occupancy
prior to cocaine administration have

A

greater
euphoric effects.

89
Q

Reinforcing effects of cocaine - Cocaine use in humans leads to
addiction in

A

10-15% of users

90
Q

Several studies have shown that
given free choice rats will choose

A

sweetened water over cocaine
infusion

91
Q

Cocaine psychosis

A

transient paranoid psychosis with delusions and hallucinations

92
Q

Cocaine psychosis Occurs more frequently over

93
Q

Cocaine psychosis Similar to psychosis in

A

Schizophrenia

94
Q

Cocaine psychosis Similar to psychosis in Schizophrenia Sensitive to

A

antipsychotics – mesolimbic DA

95
Q

Acute tolerance

A

Chronic cocaine infusion reduces the locomotor effects of a single cocaine injection

96
Q

Chronic sensitization

A

Daily injection of cocaine results in increased stereotypic behaviours in rats over time (head bobbing, corner-to-corner motion, and vertical rearing/nose poking).

97
Q

Tyrosine hydroxylase regulates overall rate of

A

catecholamine
synthesis

98
Q

Phosphorylation Activity-dependent activation

A

(CaM-kinase
phosphorylation)

99
Q

Acute tolerance results in large part from
inhibition of

A

dopamine biosynthesis

100
Q

Presynaptic autoreceptors respond to prolonged

A

DA in the synapse to inhibit TH

101
Q

Phosphorylation Modulatory activation

A

(such as PKC signalling
)

102
Q

Adverse effects of cocaine use

A

Chronic, heavy cocaine use is associated with a mild cognitive impairment

103
Q

mild cognitive impairment

A

Verbal memory, attention, and motor function

104
Q

mild cognitive impairment and grey and white matter

A

Correlated with gray and white matter abnormalities in the cortex and striatum

105
Q

Cardiotoxic effects of chronic use

A

Arrhythmia, cardiac myopathy, myocardial infarct

106
Q

Administration-dependent effects - intranasal

A

– Perforation of the nasal septum (cocaine HCl)

107
Q

Administration-dependent effects - Smoking

A

‘crack lung

108
Q

‘crack lung

A

scarring and damage to lung tissue due to vasoconstriction
of vessels in lung

109
Q

Addiction treatment

A

Animal work has been used to
evaluate the usefulness of dopamine
receptor antagonists as treatment for
cocaine addiction

110
Q

D1- and D2-family receptor
antagonists can reduce

A

reinforcing
effects of cocaine

111
Q

Specific D3 antagonists (SB-277011-
A) or partial agonists (BP897)
decrease

112
Q

Administration of ecopipam, a D1-
family antagonist, in cocaine users has
had mixed results

A

Reported to reduce high in IV trials
Reported to increase high in freebase
smoking trial

113
Q

Trials of selective DAT inhibitors or D1
agonists as replacement therapeutics
have been limited by

A

decreased seizure
thresholds

114
Q

Some studies have used disulfuram to
treat cocaine abuse due to the high
coincident use of

A

alcohol and cocaine

115
Q

Disulfuram is a common treatment for

A

alcohol abuse

116
Q

Disulfuram is a common treatment for
alcohol abuse – it inhibits

A

aldehyde dehydrogenase and causes an acute aversive reaction

117
Q

most common treatments of cocaine use are

A

antidepressants

118
Q

Fluoxetine (SSRI) treatment for cocaine addiction

A

increases 5-HT

119
Q

Desipramine (TCA) - treatment for cocaine addiction

A

increases NE

120
Q

Vaccination

A

Vaccination against small molecules is technically
possible

121
Q

Circulating antibodies would be capable of
inactivating

A

cocaine before it reaches the brain

122
Q

vaccination - Lack of effect would lead to extinction of

A

drugseeking behaviours

123
Q

vaccination - Drug molecules are covalently attached to the

A

surface of an immunogenic protein

124
Q

Immune system develops antibodies against

A

drug
molecules

125
Q

Vaccine efficacy - In animal trials cocaine vaccination

A

reduces response to drug (locomotion,
stereotypies)

126
Q

In clinical trials vaccination reduced

A

the number of cocaine users

127
Q

Vaccine efficacy Reduces effects without

A

altering
craving or impulse to use

128
Q

Vaccine efficacy Requires regular

A

boosters as cocaine is
not itself immunogenic

129
Q

Requires regular boosters as cocaine is
not itself immunogenic

A

need to
maintain high antibody levels

130
Q

While dopamine is known to regulate reinforcement in addictions, and cocaine strongly affects DAT function, dopamine transporter knockout mice (DAT -/-) still

A

readily acquire cocaine self-administration

131
Q

5-HT compensates for

132
Q

5-HT is proposed to play a role in

A

modulating reinforcement

133
Q

DAT and SERT double knockouts abolished the

A

reinforcing effects of cocaine

134
Q

Both DAT and 5-HT can play a role in reinforcing behaviours via

A

NAc DA release

135
Q

In the DAT -/- (but not wild-type) mice, fluoxetine, citalopram (SSRI), and cocaine were shown to

A

increase VTA activity leading to NAc DA release

136
Q

developmental alterations of dopamine function lead to

A

compensatory changes in 5-HT in reinforcement

137
Q

Collectively this suggests that developmental alterations of dopamine function lead to compensatory changes in 5-HT in reinforcement

A

Function switches from aversive to rewarding in the DAT -/-

Neuro-pharmacology (26 decks)

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