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Neuro-pharmacology > Norepinephrine > Flashcards

Norepinephrine Flashcards

1
Q

norepinephrine synthesis

A

L-tyroseine —TH–> L-DOPA —DOPA decarboxylase –> dopamine –DBH–>norepinephrine — PNMT –> epinephrine

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2
Q

Catecholamine breakdown occurs by

A

MAO or COMT

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3
Q

Major metabolic end-products from norepinephrine breakdown are

A

(VMA), (MHPG).

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4
Q

Levels of MHPG in the CSF or VMA in urine can be used to assess

A

catabolism of catecholamines.

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5
Q

Noradrenergic synapse NE is synthesized in

A

in vesicles from dopamine via dopamine-β-hydroxylase (DβH).

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6
Q

Noradrenergic synapse After release, NE is

A

recylced into the cell by the NE transporter (NET).

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7
Q

NE is catabolised by

A

NE is catabolised by

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8
Q

Norepinephrine and epinephrine bind and activate

A

adrenergic receptors

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9
Q

Metabotropic receptors

A

G-protein coupled

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10
Q

adrenergic receptors Responsible for both

A

CNS effects (neurotransmitters) and peripheral effects (autonomic / hormones)

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11
Q

adrenergic receptors Function as

A

post-synaptic receptors and as presynaptic autoreceptors

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12
Q

Agonists of adrenergic receptors are

A

sympathomimetic

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13
Q

Antagonists of adrenergic receptors are

A

sympatholytic

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14
Q

α1 – coupled to

A

Gqα

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15
Q

α2 – coupled to

A

Giα

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16
Q

Phenylephrine is

A

is selective agonist (α1/2)

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17
Q

α1 – coupled to Gqα
α2 – coupled to Giα

A

Vasoconstriction

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18
Q

Agonists at α2 receptors can

A

lower blood pressure – CNS acting

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19
Q

α2 receptors in the brainstem (vasomotor centre) are

A

autoreceptors

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20
Q

Clonidine prescribed to treat

A

hypertension

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21
Q

β1 – coupled to

A

Gsα

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22
Q

β2 – mostly coupled to

A

Gsα

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23
Q

β3 – coupled to

A

Gsα

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24
Q

Isoprenaline is

A

is selective agonist (β1/2/3)

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25
Q

β1 – coupled to Gsα
β2 – mostly coupled to Gsα
β3 – coupled to Gsα

A

Vasodilation

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26
Q

Agonists at β-adrenergic receptors

A

relax bronchial muscles

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27
Q

Albuterol

A

is a specific β-adrenoceptor agonist used to treat asthma

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28
Q

Metoprolol is a selective

A

β1 receptor antagonist (β-blocker) used to treat arrhythmia and angina pectoris

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29
Q

Noradrenergic projections emanate from the

A

the locus coeruleus

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30
Q

locus coeruleus

A

Small region (3000 neurons), big impact on behaviour

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31
Q

Noradrenergic projections innervate regions involved in

A

arousal, attention, and vigilance

32
Q

Norepinephrine affects

A

eating behaviours

33
Q

Paraventricular nucleus (hypothalamus) tell you when youre

A

hungry/not

34
Q

Noradrenergic pathways innervate areas involved in

A

depression

35
Q

Noradrenergic pathways innervate areas involved in depression

A

Limbic cortex, amygdala, hippocampus

36
Q

LC adrenergic neurons part of the

A

reticular activating system

37
Q

LC adrenergic neurons part of the reticular activating system

A

Fire when awake or slow wave sleep
Inactive in REM sleep
Slow breakdown of NE might account for latency during changes of consciousness

38
Q

Selective agonists for α and β adrenoreceptors increase awake time when microinjected into the

A

medial septum. indicating that both receptor systems are involved in normal functioning.

39
Q

Antidepressants Can act on

A

adrenergic receptors (predominantly α1)

40
Q

Antidepressants Often target

A

norepinephrine reuptake or breakdown

41
Q

Monoamine neurotransmitters are a common target for

A

antidepressants

42
Q

MAOI antidepressants reduce the breakdown of

A

all monoamine NTs (dopamine, norepinephrine, serotonin)

43
Q

The Monoamine Hypothesis

A

Depression is a result of a functional deficit of the neurotransmitters norepinephrine and serotonin (5-HT) at specific synapses in the CNS

44
Q

First antidepressant was a

A

a monoamine oxidase inhibitor (MAOI), iproniazad, an anti-tuberculosis drug (1952)

45
Q

MAOI cause elevation of

A

monoamines by inhibiting their catabolism

46
Q

Elevated monoamines leads to increases in

A

monaminergic neurotransmission (dopamine, norepinephrine, serotonin[ 5-HT])

47
Q

Phenylzine was the most common

A

MAOI in use clinically
Discontinued due to the cheese effect

48
Q

Imipramine (Tofranil) is an

A

inhibitor of both norepinephrine transporters (NET) and 5-HT transporters (SERT)

49
Q

Sustained NE/5-HT levels lead to

A

prolonged and increased post-synaptic activity

50
Q

Side effects on muscarinic receptors (anti-cholinergic)

A

Parasympatholytic – dry mouth, constipation, urinary retention

51
Q

Poor safety margin

A

induces mania at higher doses

52
Q

SSRI

A

Selective serotonin reuptake inhibitors

53
Q

Fluoxetine (Prozac, 1987)

A

SSRI

54
Q

SSRI actions

A

5-HT accumulates in the synapse, enhancing post-synaptic activity

55
Q

SNRI

A

Serotonin-norepinephrine reuptake inhibitors

56
Q

First SNRI was

A

venlafaxine (Effexor, 1994)

57
Q

SSRI Selective inhibitors for

A

SERT

58
Q

SNRI Inhibits both

A

SERT NET

59
Q

SNRI Fewer

A

side effects than TCAs, improved safety margin

60
Q

Challenges to the Monoamine hypothesis

A

Pharmacologic effects are very rapid (hours-days) but therapeutic effects are slow (weeks-months)
Monoamines normalize rapidly, but mood normalizes slowly

61
Q

efficacy of drugs that do not affect NA/5-HT reuptake

A

Tianeptine, a selective serotonin reuptake enhancer is equally effective as SSRIs in clinical trials

62
Q

Cocaine (potent NA reuptake inhibitor)

A

does not have antidepressant effects

63
Q

Norepinephrine reuptake inhibitors represent the third class of

A

2nd generation antidepressants brought to market

64
Q

Norepinephrine reuptake inhibitors represent the third class of 2nd generation antidepressants brought to market First was

A

reboxetine (Edronax/Prolift) in 1997

65
Q

NE reuptake inhibitors are

A

psychostimulants

66
Q

NE reuptake inhibitors are psychostimulants

A

Absence of activity at the dopamine transporter prevents addictive effects of psychomotor stimulants (e.g. cocaine)

67
Q

Noradrenergic drugs have been demonstrated effective in treating

A

attention deficit hyperactivity disorder (ADHD)

68
Q

Clonidine

A

α2A agonist increases NE tone in the PFC

69
Q

Reboxetine

A

NET inhibitor

70
Q

Clonidine – α2A agonist increases NE tone in the PFC
Reboxetine – NET inhibitor

A

Thought to act to increase / prolong NE signalling to cortex, affecting attention

71
Q

Withdrawal from opioids (heroin, morphine) activates the

A

noradrenergic system

72
Q

Withdrawal from opioids (heroin, morphine) activates the noradrenergic system

A

Responsible for withdrawal effects such as increased heart rate, elevated blood pressure, and diarrhea

73
Q

α2 receptors are targets to treat symptoms of

A

opioid withdrawal

74
Q

Clonidine is an

A

α2 agonist that is used clinically to treat opioid withdrawal symptoms

75
Q

α2 receptors in the brainstem function as

A

presynaptic autoreceptors on noradrenergic cells – activation decreases the release of NE

76
Q

Yohimbine

A

is an α2 antagonist that can be used experimentally to increase/provoke withdrawal symptoms

77
Q

IV administration of yohimbine

A

rapidly increases the severity of opioid withdrawal, and increases anxiety in patients (sometimes to the point of panic attacks), suggesting NE may also be involved in generating feelings of anxiety. Many antidepressants also have anxiolytic activites.

Neuro-pharmacology (26 decks)

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