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Neuropharmacology > Lecture 8 > Flashcards

Lecture 8 Flashcards

1
Q

What is an example of a catecholamine?

A
  • noradrenaline - dopamine
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2
Q

What is an example of a tryptamine?

A

Serotonin

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3
Q

What does noradrenaline regulate?

A
  • arousal/wakefulness/alertness (forebrain) - mood (amydgala/hippocampus) - pain control (spinal cord) - BP/autonomic function (hypothalamus)
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4
Q

What does dopamine regulate?

A
  • motor control (nigrostriatal system) - behaviour/mood (mesolimbic/mesocortical systems) - endocrine control (tuberohypophyseal system)
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5
Q

What are the dopamine receptors which are D1-like?

A
  • D1 - D5
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6
Q

Which G-protein does D1-like receptors bind to?

A

G𝛼s

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7
Q

What are the second messengers of D1-like receptors?

A

(Increased activity of) cAMP and PKA

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8
Q

What are the dopamine receptors which are D2-like?

A
  • D3 - D4
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9
Q

Which G-protein does D2-like receptors bind to?

A

G𝛼i

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10
Q

What are the second messengers of D2-like receptors?

A
  • (reduced activity of) cAMP and PKA - Gβ𝛾 decreases voltage-gated Ca2+ channels - Gβ𝛾 opens K+ channels
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11
Q

What are the physiological responses of dopamine activation?

A

increase BP + heart rate

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12
Q

What does serotonin regulate?

A
  • sleep, wakefulness and mood - feeding behaviour - control of sensory transmission
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13
Q

What is the physiological response of 5-HT receptor activation?

A
  • feeding - mood/behaviour (antidepressants) - sleep/wakefulness - control of sensory pathways (hallucinations) - pain (migraine) - body temperature
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14
Q

What is the physiological response of 5-HT3 activation?

A

Vomiting (chemotherapy)

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15
Q

What G protein does 5-HT1 bind to?

A

G𝛼i

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16
Q

What are the typical second messengers of G𝛼i activation?

A
  • (reduced activity of) cAMP and PKA - Gβ𝛾 inhibits voltage-gated Ca2+ channels - Gβ𝛾 opens K+ channels
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17
Q

What G protein does 5-HT2 bind to?

A

G𝛼q

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18
Q

What are the typical second messengers of G𝛼q?

A
  • Protein Kinase C - Ca2+
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19
Q

What G protein does 5-HT4, 5, 6 and 7 bind to?

A

G𝛼s

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20
Q

What are the typical second messengers of G𝛼s?

A

(Increased activity of) cAMP and PKA

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21
Q

What is 5-HT3 receptor bound to and what are the second messengers?

A
  • ion channel - Na+ - Ca2+
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22
Q

Where do psychoactive drugs target monoamine uptake?

A
  • plasma membrane - synaptic vesicle
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23
Q

What are the effects of psychoactive drugs on monoamine uptake?

A

Monoamine accumulation in the cleft

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24
Q

What transporter does cocaine inhbit?

A

DAT (dopamine)

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25
Q

What transporter does MDMA target?

A
  • SERT (serotonin) - taken up into the presynaptic terminal - VMAT
26
Q

What transporter does amphetamine target?

A
  • NET (noradrenaline) - taken up into presynaptic terminal - VMAT
27
Q

What enzyme does amphetamine inhibit?

A

Monoamine oxidase

28
Q

What are the main effects of amphetamines?

A
  • increased motor activity - euphoria and excitement - insomnia - anorexia
29
Q

What is a mental effect of prolonged amphetamine use?

A

Amphetamine psychosis which resembles symptoms of schizophrenia

30
Q

What are the clinical uses of amphetamines?

A
  • ADHD (adderall, ritalin) - narcolepsy (adderall, ritalin) - obesity (methedrine)
31
Q

What are the main effects of cocaine?

A
  • increased motor activity - euphoria - increased peripheral sympathetic activity (increased BP, HR)
32
Q

What are the main effects of modafinil?

A
  • increased wakefulness and vigilance
33
Q

Where does modafinil bind to?

A

Low affinity to DAT and NET

34
Q

What are examples of cognitive enhancers?

A
  • caffeine - modafinil - methyphenidate - ampakines
35
Q

What are cognitive enhancers used for?

A
  • reduce mental fatigue - maintain attention and concentration - increase motivation - alter (enhance) memory processing - normalise behaviour e.g. schizophrenia, autism
36
Q

How do ampakines work?

A
  • enhance glutamate AMPA activation - promote release of brain-derived neurotrophic factor (BDNF)
37
Q

What is the monoamine theory of depression?

A
  • drugs that enhance MA levels improve mood and symptoms of depression - vice versa for drugs lowering MA levels e.g. reserpine
38
Q

List brain areas associated with depression

A
  • amygdala - basal forebrain - cerebellum - hypothalamus - nucleus accumbens - prefrontal cortex - striatum - thalamus
39
Q

What are the types of antidepressant drugs?

A
  • monoamine oxidase inhibitors - monoamine uptake inhibitors
40
Q

What are the types of MA uptake inhibitors called?

A
  • tricyclics - selective - dual action
41
Q

What do monamine oxidase inhibitors target?

A
  • monoamine oxidase (prevents MA breakdown) - e.g. phenelzine
42
Q

Do tricyclic antidepressents target NET or SERT?

A
  • both - e.g. imipramine
43
Q

What are examples of selective monoamine uptake inhibitors?

A
  • citalopram - fluoxetine (Prozac) - reboxetine
44
Q

How do dual action monoamine uptake inhibitors work?

A
  • target both NET and SERT (SNRI) - e.g. duloxetine
45
Q

What are the areas associated with dopamine in schizophrenia?

A
  • mesolimbic pathway (positive symptoms) - mesocortical symptoms (negative and cognitive symptoms) - nigrostriatal system (motor symptoms from drug therapy) - tuberohypophyseal (hormonal disturbance from drug therapy)
46
Q

What are the positive symptoms of schizophrenia?

A
  • delusions/paranoia - hallucinations - disordered thoughts - abnormal behaviour e.g. stereotyped movements - catatonia/immobility
47
Q

What are the negative symptoms of schizophrenia?

A
  • social withdrawal - flattening of emotion - anhedonia - apathy
48
Q

What are examples of first-generation antipsychotic?

A
  • chlorpromazine - haloperidol
49
Q

Where do first-generation antipsychotics target?

A

D1 and D2 receptors (but has other targets)

50
Q

What are examples of second-generation antipsychotics?

A
  • clozapine - risperidone
51
Q

Where do second-generation antipsychotics target?

A

Some D1 activity but most at D2

52
Q

What are some side effects of antipsychotic drugs?

A
  • motor effects - increased prolactin secretion (gynecosmastia and galactorrhea) - weight gain - sedation/drowsiness
53
Q

What are the motor effects of antipsychotic drugs?

A
  • extrapyramidal effects - D2 receptor antagonism (nigrostriatal pathway) - involuntary movements/spasms/tremor (Parkinson’s symptoms) - acute dystonias (reversible) - tardive dyskinesia (irreversible)
54
Q

What are the areas associated with dopamine in Parkison’s?

A
  • tuberohypophyseal pathway - mesocortical pathway - mesolimbic pathway - nigrostriatal pathway - substantia nigra (loss of neurones)
55
Q

What are the symptoms of Parkinson’s?

A
  • suppression of voluntary movements (bradykinesia) - tremor at rest - increased resistance in passive limb movement - variable degree of cognitive impairment
56
Q

What are the two therapies used to treat Parkinson’s disease?

A
  • drug therapy - deep-brain stimulation
57
Q

What is deep brain stimulation?

A

Parkinson’s disease treatment where an electrical device is planted in the brain to stimulate structures and decreases PD symptoms.

58
Q

What are examples of drugs that act in the periphery to treat Parkinson’s?

A
  • carbidopa - benserazide - entacapone - tolcapone
59
Q

How do drugs in the periphery help treat Parkinson’s?

A

Prevent conversion of levodopa to - dopamine (carbidopa, benserazide) - 3-MethylDopa (entacapone, tolcapone)

60
Q

What are examples of drugs that act in the brain to treat Parkinson’s?

A
  • selegillline - rasagiline - tolcapone
61
Q

How do drugs in the brain help treat Parkinson’s?

A

Prevent conversion of dopamine to - DOPAC (selegiline, rasagiline)

62
Q

What are examples of agonists at D1 and D2 receptors?

A
  • pramipexole - ropinirole - rotigotine - bromocriptine - apomorphine

Neuropharmacology (15 decks)

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