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Behavioural Pharmacology > Chapter 10: Psychomotor Stimulants > Flashcards

Chapter 10: Psychomotor Stimulants Flashcards

1
Q

What spanish explorer found incas chewing coca leaves in the Andes mountains in 1531?

A
  • Francsisco Pizzaro
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2
Q

In the 1500s conquistadors use coca as a what to exploit and subjugate their inca labourers?

A

reward

positive reinforcer

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3
Q

In 1786 Lamarck classified the coca plant as what?

A
  • Erythroxylon coca
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4
Q

In 1860 Albert Niemann isolated the active alkaloid of the coca leaf and called it what?

A

cocaine

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5
Q

In 1883 Angelo Mariani introduced what which had cocaine in it?

A

Mariani’s Wine

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6
Q

In 1884 _______ prescribed cocaine for his friend to aid in his morphine addiction..

A

Sigmund Freud

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7
Q

In 1884 Sigmund Freud also wrote a book on cocaine explaining what?

A
  • the virtues of it
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8
Q

By 1884 Karl Koller wrote a medical paper on what property of cocaine?

A

local anesthetic properties

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9
Q

In 1884 William Halstead the founder of John Hopkins Med School did what?

A

experimented with cocaine injections to aid with his morphine addiction

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10
Q

In 1886 what was invented by John Smythe Pemberton?

Hint: ___+ rum = smashed

A

Coca-Cola …. with active alkaloid

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11
Q

In 1887 freud recognized what about cocaine?

A
  • adverse effects of it…
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12
Q

In 1889 Magnan and Saury described what about cocaine?

A

tactile hallucinations aka coke bugs

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13
Q

By 1899 what was the cocaine mentality like?

A
  • harmful
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14
Q

In 1906 what was established?

A

Pure Food and Drug Act (US) requires accurate labelling…..coca cola goes clean…no more cocaine, now caffeine

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15
Q

In 1914 what occurred?

cocaine trafficking goes?

A

cocaine use was now regulated
- passage of Harrison Narcotics Act (US)
cocaine trafficking goes underground

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16
Q

Cocaine is derived from what?

A

Erythoxylum coca

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17
Q

1.Amphetamine (types and where do they occur)

A
  1. Synthetic
    A) d-amphetamine: more potent in central effects (ex: Dexedrine)
    B) l-amphetamine
    C) dl-amphetamine- mixture of both isomers (ex: Adderall
    - used in the treatment of ADHD and narcolepsy
    D) Methamphetamine: treats ADHD and obesity
    L> Desoxyn or Methedrine ..can be synthesized from cold medication
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18
Q

2.Methylphendate (source and example)

Pipradrol ?

A
  • slightly different from cocaine
  • synthetic
  • Ritalin
  • treats ADHD
  • – treats senile dementia
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19
Q

3.Ephedrine ( source and example)

A
  • naturally occurring

- herb–> Ma Huang

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20
Q

4.Cathinone ( source and example)
Synthetic Derivatives?
Bupropion
others have been used recreationally (3)

A
  • naturally occurring
  • Catha edulis
  • not stable
  • antidepressant and smoking cessation aid
  • Mephedrone
  • ephedrone
  • methedrone
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21
Q

5.Mephedrone ( source and example)

A

aka bath salts to avoid legal issues

synthetic from cathinone

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22
Q

On a dosage curve graph stimulants take what shape?

A

inverted U

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23
Q
  • Psychomotor drugs stimulate synapses that use what?(4)
  • collectively what are these called?
  • Which three are very similar? Collectively what are they called?
A
  • Epinephrine(E), norepinephrine(NE), dopamine(DA) and serotonin (5-HT)
  • Monoamines
  • E, NE and DA; catecholamines
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24
Q

What is an Indoleamine?

A
  • 5-HT aka serotonin
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25
Q

Sympathomimetic?(2)

think 5-HT

A
  • chemically different from CAs but influenced by many of the same drugs and destroyed by the same enzymes..
  • E is the primary transmitter in the SNS….and 5-HT stimulate sympathetic synapses mimicking sympathetic arousal
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26
Q
  • Amphetamines are what??(kpa)
  • implicating what when taken orally
  • it’s more potent when taken how?3
A
  • weak bases, kpa= 9-10
  • ionize in digestive system, slowing the rate of absorption when taken orally
  • injection, inhalation or snorting
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27
Q

What is the advantage of taking amphetamines orally?

A
  • blood levels may be kept fairly constant without too much variation over time
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28
Q

Cocaine has what kind of a Kpa?

is it similar to Amphetamines or dissimilar?

A
  1. 7

- similar in routes of administrations

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29
Q

Cocaine is nearly always taken how?

However it has recently been popular to take it how and as what?

A
  • injected, sniffed to improve absorption

- via smoke, hydrochloride salt and as a freebase

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30
Q

What is the most common form in the US to take cocaine?

A
  • hydrochloride cocaine
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31
Q

Describe Tooting!

- origin?

A
  • place some of the powder on a sheet of tinfoil and heat it until vaporized and inhale it ( similar to injection)
  • started off as a way to test purity, pure cocaine leaves little residue behind on tinfoil
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32
Q

What is crack?3

A
  • Cocaine HCl mixed with a solution of baking soda
  • water evaporates leaving crystalline chunks aka rocks..that are heated in pipes
  • baking soda is a base and removes ionic charge increasing lipid solubility of substance..
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33
Q

After oral administration the rate of absorption for amphetamines is determined by what?
Peak blood levels?

A

presence of food inn the stomach and the degree of physical activity
- peak bl= 30 mins- 4hours

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34
Q

After intranasal administration of cocaine peak bl is reached when?

A
  • 10-20 mins
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35
Q

Why is the rate of absorption for vaporized cocaine HCl and cocaine via freebase so high?

A
  • release the cocaine molecule in unionized form, making it highly lipid soluble
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36
Q

Cathinone is taken how?

A

orally via chewing leaves of Khat

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37
Q

Methacathinone is taken how in Russia? USA?

A
  • injection

- sniffing

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38
Q

Mephedrone is sold under what? and taken how?

A
  • bath salts and plant food ( powder, tablets or capsules)

- orally, injected or snorted

39
Q

All psychomotor stimulants cross what? and are in high concentration where?

A
  • blood brain barrier

- spleen, kidneys and brain.

40
Q

Psychomotor stimulants are widely distributed due to their?

A

lipid solubility

41
Q

Half life amphetamine and cocaine depend on the pH of what? why?(3)

A
  • urine
  • if the urine is acidic, since they are basic they will not be reabsorbed from the nephron
  • as urine becomes basic, more of the drug is reabsorbed and more of the excretion is handled by metabolism by the liver.
42
Q

What is the half life of amphetamine when the urine is acidic, basic?
other excretion method?

A
  • 7-14 hours; 16-34 hours

- also excreted via sweat and saliva

43
Q

What is the half life of cocaine when the urine is acidic, basic?

A
  • 45 to 75 mins in general
44
Q

Many of the metabolites of amphetamine are what?

A

behaviourally active and have very long half lives

45
Q

Cathinone has a half life of?

  • metabolized via?
  • metabolites?
A
  • 90 mins

- metabolized by three specific pathways in the liver…some toxic effects are due to accumulation of its metabolites

46
Q

After the function of monoamine transporters occur in one of two ways! ( Neurophysiology)
list the two…

A

Monoamine re-uptake inhibitor

Substrate- like releasers

47
Q

Monoamine re-uptake inhibitor??

A
  • cocaine
  • drug influences DAT,NET and SERT
  • blocks the transporters on the presynaptic cells membrane also the VMAT ( vesicular monoamine transporter)- which normally sorts the NT back into a vesicle
48
Q

Substrate-like releasers???

3 examples as well!

A
  • amphetamine, methcathinone and cathinone
  • competition between NE and amphetamine; slows it down
  • amphetamine tries to get through the NET stopping/slowing down NE from getting back in
  • leaving more NE in the synaptic cleft
  • once amphetamine gets into the cell it forces NE out of the cell via reverse motion
49
Q

Once amphetamines are re-absorbed into the vesicles of the presynaptic cell they disrupt what?
(Substrate-releasers)

A
  • vesicular pH balance which triggers the vesicles to release monoamines into the cytoplasm
50
Q

With the increased [Na+] in the presynaptic cell what occurs?(substrate-like releasers)

A
  • causes the transporter proteins to work in reverse order..moving monoamines out of the cell
  • this is done by blocking VMAT and prevents the storage of monoamines
51
Q

Amphetamines also inhibit what activity in the presynaptic cell???? (substrate-like releasers)

A
  • MAO enzyme activity…preventing monoamines to be degraded in the presynaptic cells cytoplasm..
52
Q

On the presynaptic cell what is not working on the membrane with Substrate-like releasers??

A
  • auto receptors which normally modulate the amount of NT in the synaptic cleft…
53
Q

What transporters are affected by Cocaine, Methylphenidate, Amphetamine and Mephedrone

A
  • Cocaine: NET DAT and SERT
  • Methylphenidate: NET and DAT, to a minor extent SERT
  • Amphetamine: NET and to a lesser extent DAT and SERT
  • Mephedrone: Largely SERT
54
Q

In the PNS the release of epinephrine causes what?

A

sympathomimetic effects

55
Q

Cocaine blocks what ? Preventing what? Resulting in what?

A
  • sodium ion channels, action potentials

- local anesthesia

56
Q

Enactogens have a high affinity for what??ex?

A

SERT, MDMA - ecstasy

57
Q

Effects on the body??(3)

A
  1. appetite reduction- via stimulating behaviour other than eating! preoccupied aka secondary effect.This is compensated for later by binging !
  2. Vasodilation: increase in heart rate and BP
  3. Bronchodilation: dilation of air passages of the lungs…improves breathing
58
Q

Effects on sleep? (2)

Amphetamines??? Popular among? can cause?

A
  1. reduce fatigue and block sleep onset
  2. used in the treatment of narcolepsy
    L> amphetamines increase concentration: students! can cause insomnia
59
Q

Subjective effects?? (3)

A
  1. Improve mood
  2. Produce euphoria at high doses after intravenous or intranasal administration; rush is described in sexual terms, within seconds of admin lasting aprox 45 seconds (orgasm)
  3. Intravenous cocaine exp found that, euphoria occurs within the first 10-15 mins but the presence of the drug can be detected for 75 mins.
60
Q

Over repeated exposure to cocaine intravenously what remained constant, what disappeared?

A
  • positive feelings aka feeling good, rush disappeared
61
Q

Stereotyped Behaviours??? (2)
term
cause
L>disease?

A
  1. punding (repetitive behaviours - humans) - won’t go to the bathroom, eat or drink during this….annoyed if disrupted
  2. Caused via drugs acting on the nigrostriatal DA system.. ( deteriorates during Parkinson’s Disorder)
62
Q

Monoamine Psychosis?
A. Similar to what Psychotic symptom disorder?
B. Formication?

A

A.Paranoid Schizophrenia
- auditory hallucinations and visual
- delusions of persecution
- delusions of grandeur
- hostility/violence due to paranoia–> unpredictable and sudden
-depression, anxiety - crashing symptoms
B. feeling of creatures crawling on skin/under

63
Q

DIfference between heroine and speed users?

A

heroine users= crimes of theft

speed users= crimes of violence via paranoia

64
Q

Sensory Effects? (2)

A
  1. increased visual acuity
  2. passage of time is underestimated…1 minute seems longer than it actually is..this is due to more heartbeats in a minute than their normally would be..brain misinterprets this as a longer passage of time.
65
Q

Effects on performance? (4 there is another but included on another slide..)

A
  1. improved task performance degraded by fatigue (reaction time)
  2. improvement in complex motor skills vs simple ones
  3. improvement in taks required vigilance or prolonged attention
  4. enhanced athletic performance (endurance type activities)
66
Q

Effects on performance continued….in relation to ADHD? (4)

A
  1. improves attention( inhibition of processing of irrelevant stimuli)
  2. reduces hyperactivity and impulsivity
  3. not all children/ adults respond to stimulants
  4. not a paradoxical effect, thought to stimulate a hypoactive prefrontal cortex.( works via stimulating DA and noradrenergic activity…improving attention and impulse control)
67
Q

Describe the example experiment the Prof gave in class: GO.
Treatment phase?
Washout phase? Importance? What about experiments that don’t include this?
Test phase? - Trial 1 and 2
Results?

A

-Young rats were trained to eat hard rat chow and powder chow ..
-Treatment phase: 5mg/kg MPH (Ritalin) oral admin via powder chow only on week days (same as children treatment) - weekends off.
L> this was done for 27 days…twice a day (42 doses total)
- Washout phase: 10 to 15 days to get it out of system (see if changes in the brain remain after drug is gone)
Test Phase:
- Trial one–> placed in an open field with to similar objects..allowed to explore for ~3 hours.. measuring the amount of time at each
- Trial two—> familiar object + novel object…animal is measured spending more time with the novel (this depends on intermediate memory)
Results: three hours after test…they are spending time at both…indicating they lack intermediate memory of observing the familiar object….by 15 days they are exploring both at the same amount of time..
**without washout period this is not seen.

68
Q

Performance Deficits ?

2

A
  1. stimulants cause the user to focus on only one feature of the environment - tunnel vision
  2. at higher doses people become impatient, are easily distracted and show impaired judgment
69
Q

Effects on driving?
(2)
Silber et al. (2005)

A
  1. amphetamines : drift out of the lane, drive erratically, weave, speed, increased risk of collision
  2. Silber et al. (2005)
    - failure to stop at red lights
    - slow reaction times…not muscular, attention! .
    ( this was seen during day time not night!) night seemed to have no effect!
70
Q

Effects on non-humans ?

4

A
  1. stereotyped behaviours
  2. automutilation
  3. decreased eating and drinking
  4. Rate-dependency effect: increased responding on FI but decreased responding on an FR schedule….at the same dosage.
71
Q

Dissociation ( state dependency) ?

A

memory consolidation issues; cannot recall tasks performed while under the influence of the drug..

72
Q

Drug State Discrimination?
Humans?
Animals?
Rats distinguished via?

A
  • In humans: methamphetamine and d-amphetamine could not be distinguished (became generalized) but triazolam could be!
  • Animals generalize: amphetamine to cocaine, methylphenidate, cathinone, and some monoamine oxidase. (MAO)
  • Rats: do not generalize amphetamines to caffeine, nicotine, barbs, chlorpromazine, atropine or any common hallucinogens.
73
Q

Acute Tolerance? (2)

A
  1. Develops to subjective effects

2. does not develop to BP and heart rate

74
Q

Chronic Tolerance ? Sensitization? (3)

A
  1. rapid tolerance to appetite suppression and lethal effects
  2. no tolerance to the sleep disrupting effects
  3. Sensitization causes increase in stereotypy and locomotion (psychotic behaviour as well)
75
Q

Withdrawal?

A
  1. not associated with a severe or medically serious withdrawal
  2. depression and lethargy are the most prominent
  3. after chronic heavy use, appears within 24 hours of cessation
  4. depression is similar to psychiatric symptoms
  5. Dysfunction of prefrontal cortex: with impaired cognitive and memory functions can last for ~ 1 year.
76
Q

What is the difference between psychiatric depression and withdrawal depression via amphetamine ?

A
  • amphetamine induced depression causes an increase in sleep and appetite whereas psychiatric depression causes the opposite.
77
Q

Withdrawal onset for cocaine?

Amphetamine?

A
  • half an hour ( rush is followed by a crash/ comedown- lethargy and depression)
  • delayed for many hours
78
Q

Initial phase for withdrawal can last for a week but what can last for weeks to months?

A
  • increased appetite, sleep disturbances and depression
79
Q 
Self Administration in humans? 
Cocaine? (3)
Rub-asbtinence cycle? 
combination?
L> compensatory combination of drugs?
A
  1. Run/crash= Run-abstinence cycle: snorted or injected in large quantities followed by by periods of abstinence.
  2. often combined with other drugs
  3. Speedball: cocaine and heroin ( reduces jitteriness from cocaine, cocaine reduces the sleepiness or nod caused by heroin )
80
Q 
Self Administration in Humans? 
Amphetamines (3)
common with cocaine? 
low doses 
high doses 
L> crash?
A
  1. run-abstinence cycle is present but sporadically not continuously like with cocaine…because amphetamine is longer lasting( constant Blood lvls)
  2. used in low doses by those who wish to stay awake, truck drivers, soldiers, students etc
  3. high doses = euphoric effects ….followed by a crash and 24-48 hours of sleep
81
Q

Self administration in non humans (2)

A
  1. when continuously available , lethal effects may be reached
  2. when use is restricted - doses are limited via use…restraint is shown. (rats)
82
Q 
Harmful effects ? 
Direct effects (4)
A
  1. liver damage
  2. inflammation and ulceration of the mucous membranes in the nose
  3. neurotoxic effects on dopaminergic cells
  4. chronic methylphenidate can yield memory deficits in rats
83
Q

Harmful effects?

Indirect? (4)

A
  1. illnesses arise from tweaker’s life style: poor diet , lack of sleep
  2. higher death rate
  3. HIV and AIDS increase via dirty needles
  4. suspicious, antisocial and prone to violence
84
Q

Harmful Effects:

Reproduction? (3)

A
  1. low doses increase sexual performance
  2. high doses impair sexual interests
  3. children of mothers who used cocaine while pregnant have higher behavioural problems: low attention span and high aggression and irritability.
85
Q

Harmful Effects:

Overdose? (2)

A
  1. absolute dose is not as important as sudden increase in drug lvld in the brain
  2. strain- difference in cocaine induced lethality in rats suggest genetic differences in sensitivity to cocaine in humans.
86
Q

Caine reaction?(2)

treatment?(2)

A
  • initial excitement followed by severe headaches, nausea, vomiting and severe convulsions.
  • followed by loss of consciousness, respiratory depression, and then finally cardiac failure causing death. (2-3 mins or to a half an hour before death)
  • diazepam: seizures and respiratory depression
  • Chlorpromazine: antipsychotic that treats toxic effects
87
Q

Treatment :

-Behavioural Therapies?(3) most effective? rank them.

A

-Cognitive Behaviour Therapy: teaches strategies to think rationally, avoid maladaptive thinking and prevent relapse (most effective)
- Contingency management: conditioned rewards for operant conditioning
- Community Reinforcement: social reinforcement like praise and encouragement for abstinence
CBT>Con>com

88
Q

Treatment:

Modafinil (3)

A
  • stimulates DA, norepinephrine,and GA transmission….as well as histamine
  • cognitive enhancer, treat ADHD, narcolepsy
  • limite abuse potential banned for athletes..
89
Q

Treatment:

Bupropion?(4)

A
  • antidepressant
  • smoking cessation
  • DAT and NET blocker
  • reduces craving for methamphetamine users…only in light users
90
Q

Treatment:

Methylphenidate?(5)

A
  • ritalin
  • treat ADHD
  • blocker of DAT and NET little effect on SERT
  • less abuse potential than cocaine and amphetamine
  • reduce use in heavy intravenous amphetamine users
91
Q

Treatment :

Oral d-amphetamine(3)

A
  • no huge fluctuations in blood level, (euphoria cause)
  • increased treatment retention
  • decreased methamphetamine consumption
92
Q

Treatment:

Naltrexone?(2)

A
  • opioid antagonist
  • reduce the cue induced reinstatement of methamphetamine self administration in lab animals and to block the subjective effects of d-amphetamine and craving in amphetamine dependent addicts.
93
Q

What are the three drugs that have proven to be successful in a double blind exp along with d-amphetamine?

A
  • bupropion, modafinil and naltrexone
94
Q

Immunization? HUH? vaccines?

example?

A
  • antibodies bind to molecules of cocaine
  • created via binding drug molecule to a fragment of a virus….immune system creates antibodies to both the fragment and the drug.
  • prevents people from become addicts and prevents reinforcing effects of drugs in addicts.
  • frequent boosters are needed
  • cocaine binded to adenovirus gene transfer vector - carry gene into cells.

Behavioural Pharmacology (52 decks)

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