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LF261: Neuropharmacology > Lecture 8. Psychotropics and Psychostimulants: Use and Abuse > Flashcards

Lecture 8. Psychotropics and Psychostimulants: Use and Abuse Flashcards

1
Q

What are the two main nuclei that the noradrenergic fibres of the brain stem from?

A

Locus coeruleus
Lateral tegmental area

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2
Q

What are the noradrenergic fibres in the forebrain responsible for?

A

Arousal/wakefulness/alertness

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3
Q

What are the noradrenergic fibres in the amygdala/hippocampus responsible for?

A

Mood

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4
Q

What are the noradrenergic fibres in the spinal cord responsible for?

A

Control of pain

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5
Q

What are the noradrenergic fibres in the hypothalamus & NTS responsible for?

A

Blood pressure/autonomic function

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6
Q

What dopaminergic neurones travel to the forebrain to carry out executive functioning (decision making)?

A

Ventral tegmental area

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7
Q

What dopaminergic neurones are responsible for Parkinson’s disease when they degrade?

A

Substantia nigra

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8
Q

What does the dopaminergic nigrostriatal system control?

A

Motor control

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9
Q

What do the dopaminergic mesolimbic/mesocortical systems control?

A

Behaviour/mood

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10
Q

What does the dopaminergic tuberohypophyseal system control?

A

Endocrine control

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11
Q

What are the two D₁-like dopamine receptors?

A

D₁, D₅

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12
Q

What are the three D₂-like dopamine receptors?

A

D₂, D₃, D₄

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13
Q

What G protein subtype are D₁-like dopamine receptors coupled with?

A

Gαs

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14
Q

What G protein subtype are D₂-like dopamine receptors coupled with?

A

Gαi

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15
Q

What are the typical second messengers of D₁-like dopamine receptors?

A

Increased cAMP & PKA activity

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16
Q

What are the typical second messengers of D₂-like dopamine receptors?

A

Reduced cAMP & PKA activity
Gβγ ↓voltage-gated Ca²⁺ channels
Gβγ opens K⁺ channels

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17
Q

What are the physiological responses caused by D₁-like dopamine receptors?

A

Voluntary movement (Parkinson’s disease)
Reward (drugs of abuse)

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18
Q

What are the physiological responses caused by D₂-like dopamine receptors?

A

Sleep regulation
Mood/cognition/attention (schizophrenia; ADHD)
Hormonal regulation (pituitary)
Sympathetic regulation
Nausea/vomiting

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19
Q

What is the primary nucleus responsible for the projection that produces serotonin (5-HT) within the brain?

A

Raphe nuclei

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20
Q

What 5-HT receptor subtype is not G protein coupled?

A

5-HT₃ (pentameric ionotropic receptor)

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21
Q

What physiological responses are caused by 5-HT (ignoring 5-HT₃)

A

Feeding
Mood/behaviour (antidepressants)
Sleep/wakefulness
Control of sensory pathways (hallucinations)
Pain (migraine)
Body temperature

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22
Q

What are the typical second messengers of 5-HT₃?

A

Na⁺
Ca²⁺

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23
Q

What physiological responses are caused by 5-HT₃?

A

Vomiting (chemotherapy)

24
Q

What do each monoamine neurotransmitter have?

A

Plasma membrane uptake carrier
DAT (dopamine)
SERT (serotonin)
NET (noradrenaline)

25
Q

What does cocaine inhibit?

A

Dopamine uptake, resulting in dopamine build-up

26
Q

What is the effect of MDMA on serotonin uptake?

A

MDMA causes an accumulation of serotonin in the synaptic cleft by being taken up by SERT, creating competition
MDMA competes with serotonin and is taken up by VMAT into the synaptic vesicles preventing serotonin entry

27
Q

What is the effect of amphetamine on noradrenaline intake?

A

Amphetamine causes an accumulation of noradrenaline in the synaptic cleft by being taken up by NET, creating competition
Amphetamine competes with noradrenaline and is taken up by VMAT into the synaptic vesicles preventing noradrenaline entry
Amphetamine inhibits monoamine oxidase (MAO) enzymes, preventing noradrenaline breakdown

28
Q

What are the main effects of amphetamines?

A

Increased motor activity
Euphoria and excitement
Insomnia
Anorexia

29
Q

What can occur if prolonged use of amphetamines occur?

A

Amphetamine psychosis, resembles symptoms of schizophrenia

30
Q

What amphetamines are used to treat ADHD and what are the dosages?

A

Adderall - 2.5 or 5 mg once or twice per day (< 40 mg/day)
Ritalin - < 60 mg /day

31
Q

What amphetamines are used to treat narcolepsy and what are the dosages?

A

Adderall - 5 mg to 60 mg per day in divided doses
Ritalin - < 60 mg /day

32
Q

What amphetamine is used to treat obesity?

A

Methedrine - 5 mg tablet before each meal

33
Q

What are the main effects of cocaine?

A

Increased motor activity
Euphoria, excitement and garrulousness
Increased peripheral sympathetic NS activity (↑BP, ↑HR)

34
Q

What are the main effects of modafinil?

A

Increased wakefulness and vigilance
Suggested to improve cognitive performance (likely through increased wakefulness)

35
Q

What does modafinil bind to?

A

Low affinity to DAT and to NET

36
Q

Does modafinil have a high or low abuse potential?

A

Low (no high or euphoria)

37
Q

What are the believed or hoped for effects of of cognitive enhancers?

A

Reduce mental fatigue
Maintain attention and concentration
Increase motivation (especially for dull & repetitive tasks – eg exam revision)
Alter memory processing (i.e. enhance memory)
Normalise behaviour (eg schizophrenia, autism disorders, addiction)

38
Q

What are examples of cognitive enhancers

A

Caffeine
Modafinil
Methyphenidate
Ampakines

39
Q

What are the effects of ampakines?

A

Enhance activation of glutamate AMPA receptors
Promote release of brain-derived neurotrophic factor (BDNF)
Show evidence of enhancing cognition in a range of tests

40
Q

Are ampakines on the market?

A

No

41
Q

What is the monoamine theory for depression?

A

Drugs that enhance monoamine levels improve mood and symptoms of depression and vice versa (eg reserpine) for drugs lowering monoamine levels

42
Q

What do many antidepressant drugs elevate?

A

Monoamine levels
Fluoxetine and reboxetine - monoamine uptake inhibitor (selective)

43
Q

What causes the positive symptoms of schizophrenia? (Positive not as in good)

A

Over-activity in the mesolimbic dopaminergic pathway activating dopamine D₂ receptors

44
Q

What causes the negative symptoms of schizophrenia?

A

Decreased activity in the mesocortical dopaminergic pathway (D₁ receptors)

45
Q

What are the positive symptoms of schizophrenia?

A

Delusions/paranoia
Hallucinations (voices)
Thought disorder
Abnormal behaviour (eg stereotyped movements)
Catatonia/immobility

46
Q

What are the negative symptoms of schizophrenia?

A

Social withdrawal
Flattening of emotion
Anhedonia (inability to experience enjoyment)
Apathy (eg for hygiene, routines)

47
Q

What causes the cognitive symptoms of schizophrenia?

A

Attention and memory - Mesocortical pathway

48
Q

What are examples of first class (generation, typical, classical or conventional) antipsychotic drugs?

A

Chlorpromazine
Haloperidol

49
Q

What do first class antipsychotic drugs target?

A

D₁, D₂ receptors (but other targets also)

50
Q

What are examples of second class (generation or atypical) antipsychotic drugs?

A

Clozapine
Risperidone

51
Q

What do seconds class antipsychotic drugs target?

A

Some activity at D₁, D₂
More activity at D₂

52
Q

What are the side effects of antipsychotic drugs?

A

Motor effects (Extrapyramidal effects, D₂ receptor antagonism in nigrostriatal pathway, Involuntary movements/tremor/spasms/rigidity – symptoms of Parkinson’s disease, Acute dystonias, Tardive dyskinesia)
Increased prolactin secretion leading to gynecomastia (in men) and galactorrhea
Weight gain
Sedation/drowsiness

53
Q

What is Parkinson’s disease?

A

Major neurodegenerative disorder in which patients display profound motor impairment

54
Q

What are the symptoms of Parkinson’s disease?

A

Suppression of voluntary movements (bradykinesia, muscle rigidity, motor activity is difficult to initiate and stop)
Tremor at rest, (‘pill-rolling’ tremor) “pill rolling” tremor of the hands
Increased resistance in passive limb movement
A variable degree of cognitive impairment

55
Q

What treatments are used for those with Parkinson’s disease?

A

Utilising dopamine precursors and dopamine receptor agonists

LF261: Neuropharmacology (15 decks)

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