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Nervous System > Applied Neuropharmacology > Flashcards

Applied Neuropharmacology Flashcards

1
Q

Describe the sequence of events in synaptic transmission?

A
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2
Q

step one synaptic transmission?

A

Synthesis and packaging of neurotransmitter (usually) in presynaptic terminals

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3
Q

step two synaptic transmission?

A

Na+ action potential reaches terminal

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4
Q

step three synaptic transmission?

A

Activates voltage gated Ca2+ channels

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5
Q

step four synaptic transmission?

A

Triggers Ca2+-dependent exocytosis of pre-packaged vesicles of transmitter

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6
Q

step five synaptic transmission?

A

Transmitter diffuses across cleft and binds to ionotropic and/or metabotropic receptors to evoke postsynaptic response

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7
Q

step six synaptic tranmission?

A

Presynaptic autoreceptors inhibit further transmitter release

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8
Q

step seven synaptic transmission?

A

Transmitter is (usually) inactivated by uptake into glia or neurons

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9
Q

step eight synaptic transmission?

A

transmitter is metabolised within cells

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10
Q

What are the different receptor types for neurotransmitters?

A

Ionotropic (respond to ligand binding)

Metabotropic (acts through a second messenger. It may be located at the surface of the cell or in vesicles)

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11
Q

Is acetylcholine uptaked into glia/neural cells or is it inactivated by breakdown?

A

Inactivated by enzymatic breakdown in the synaptic cleft

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12
Q

What are some methods of pharmacological manipulation to reduce synaptic transmission?

A
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13
Q

what are examples of blocking Na+ voltage gated channels?

A

local anaesthetics, lidocaine

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14
Q

what are examples of blocking Ca+ voltage gated channels?

A

black widow spider venom

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15
Q

What are some methods of pharmacological manipulation to increase synaptic transmission?

A
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16
Q

what is a pharmacological management which blocks breakdown of transmitter?

A

anti-cholinesterases

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17
Q

what is a pharmacological management which blocks uptake of transmitter

A

SSRIs

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18
Q

what is an example of pharmalogical manipulation that increases synthesis and packaging of neurotransmitter?

A

e.g. by increasing availability of precursors

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19
Q

What are examples of different neurotransmitters?

A

Acetylcholine

Monoamines
Noradrenaline
Dopamine
Serotonin (5-HT)

Amino acids
Glutamate
GABA
Glycine

Purines
ATP
Adenosine

Neuropeptides
Endorphins
CCK
Substance P
NO

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20
Q

what are examples of monoamines?

A

Noradrenaline
Dopamine
Serotonin (5-HT)

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21
Q

what are examples of amino acids?

A

Glutamate
GABA
Glycine

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22
Q

What are examples of purines that act as neurotransmitters?

A

ATP
Adenosine

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23
Q

What are examples of neuropeptides that act as neurotransmitters?

A

Endorphins
CCK
Substance P

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24
Q

A limited range of neurotransmitters means what in terms of function?

A

a single neurotransmitter has multiple functions in different regions

Often in the brain and in the peripheral nervous system – separated by the blood-brain barrier

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25
Q

What things about neurotransmitters are unique?

A

Each neurotransmitter has:

Its own anatomical distribution
Its own range of receptors it acts on
Its own range of functions in different regions (some separated by the blood brain barrier)

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26
Q

What is the anatomical distribution of dopamine?

A

Brain stem
Basal ganglia
Limbic system and frontal cortex

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27
Q

What physiological functions are affected by dopamine?

A

Voluntary movement
Emotions/reward
Vomiting

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28
Q

What four pathways does dopamine act in?

A

mesocortical pathway
nigrostriatal pathway
tubero-infundibular pathway
mesolimbic pathway

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29
Q

What is the mesolimbic pathway?

A

Projects VTA to nucleus accumbens and other limbic structures

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30
Q

What does overactivity of the mesolimbic pathway lead to?

A

Schizophrenia and hallucinations

31
Q

What is the mesocortical pathway?

A

projects to frontal cortex

32
Q

The mesolimbic pathway has a role in what?

A

Role in reward and addiction

33
Q

The mesocortical pathway has a role in what?

A

Involved in executive function

34
Q

What does the tubero-infudibular pathway do?

A

inhibits prolactin

35
Q

What is PD caused by?

A

Degeneration of DA cells in the SN (nigrostriatal)
DA deficiency in the basal ganglia

36
Q

How does PD impact dopamine?

A

Caused by degeneration of DA cells in the nigrostriatal so causes dopamine deficiency in the basal ganglia

37
Q

Describe the synthesis of dopamine?

A
38
Q

How can dopamine synthesis be modulated in vivo?

A

Pharmacologically block the conversion of DOPA to dopamine in the periphery, so DOPA crosses the blood brain barrier into the brain and is converted to dopamine there

39
Q

Are any dopamine receptors ionotropic?

A

No ionotropic receptors (so dopamine cannot evoke fast EPSPs or IPSPs)

40
Q

What class of receptors are dopamine receptors?

A

Metabotropic (ie g-protein coupled)

41
Q

How many different subtypes of metabotropic dopamine receptors are there?

A

5 subtypes named D1 - D5

42
Q

Dopamine can produce many different effects, and different effects in different brain regions. What does this depend on?

A

which receptors are expressed

43
Q

What protein are dopamine receptors coupled to?

A

D1 and D5

44
Q

What dopamine receptors inhibite adenylate cyclase?

A

D2, D3 and D4

45
Q

What are key enzymes in the breakdown of dopamine?

A

Monoamine oxidase B (MAO-B)

Catechol-O-methyltransferase (COMT)

46
Q

What is dopamine ultimately broken down into?

A

homovanillic acid

47
Q

What are symptoms of PD?

A

Stiffness, slow movements, change in posture, tremor

48
Q

What are examples of dopaminergic drugs?

A

DA precursor
Levodopa

DA agonists
Ergots:
Bromocriptine, pergolide, cabergoline
No longer used: 5-HT(2B) stimulation → fibrosis

Non-ergots
ropinirole, pramipexole, rotigotine

Apomorphine

These drugs improve some symptoms of PD

49
Q

Why are dopaminergic drugs used in the treatment of PD?

A

ease symptoms

50
Q

what is an example of a DA precursor?

A

Levodopa

51
Q

what are exampes of DA agonists?

A

Ergots:
Bromocriptine, pergolide, cabergoline
No longer used: 5-HT(2B) stimulation → fibrosis

Non-ergots
ropinirole, pramipexole, rotigotine

52
Q

What are some enzyme inhibitors used for preserve dopamine levels?

A

Peripheral AAAD inhibitors
Such as carbidopa and benserazide
Decreases peripheral side effects of levodopa and allows greater proportion of oral dose to reach CNS

MAOB inhibitors
Such as selegiline, rasagiline and safinamide

COMT inhibitors
Such as entacapone and opicapone
Decreases metabolism of dopamine and increased effectiveness of levodopa

53
Q

Peripheral AAAD inhibitors examples?

A

carbidopa and benserazide

54
Q

effect of Peripheral AAAD inhibitors?

A

Decreases peripheral side effects of levodopa and allows greater proportion of oral dose to reach CNS

55
Q

examples of MAOB inhibitors?

A

Such as selegiline, rasagiline and safinamide

56
Q

examples of COMT?

A

Such as entacapone and opicapone

57
Q

effect of COMT?

A

Decreases metabolism of dopamine and increased effectiveness of levodopa

58
Q

what do enzyme inhibitors have no effect on?

A

synthetic dopamine agonists

59
Q

Drug treatment of PD targets what?

A

Dopaminergic neurons

60
Q

What are some possible side effects of dopaminergic drugs?

A

Worsen or cause
Nausea
Vomiting
Psychosis
Impulsivity/abnormal behaviours

61
Q

Dopaminergic drugs improve what?

A

Some motor features of Parkinson’s
e.g. limb rigidity & bradykinesia, tremor

62
Q

what do Dopaminergic drugs fail to help?

A

“Midline” features
eg dysathria, balance, cognition.

63
Q

what do dopmaine antagonists improve?

A

Nausea
Vomiting
Psychosis

64
Q

what can dopamine antagonists worsen or cause?

A

Parkinsonism

65
Q

How can antagonitsts that do not cross the blood brain barrier improve vomiting?

A

Area postrema (vomiting centre) is in the medullar and functionally outside the blood brain barrier

66
Q

What is the vomiting centre called?

A

Area postrema

67
Q

What drug is used to treat vomiting in PD patients?

A

Domperiodne
DA antagonist
Anti-emetic
Does not cross blood brain barrier
No antipsychotic properties
Relatively safe to use in PD
Has permitted the therapeutic use of apomorphine (which is a powerful emetic)

68
Q

What is dyskinesias?

A

Abnormal involuntary movements

69
Q

Which of DA agonists and DA antagonists cause dyskinesias?

A
70
Q

What can long term DA antagonist use lead to?

A
71
Q

GABA agonists are used to treat what?

A

Anti-epilepsy drug

Also have anti-anxiety properties

72
Q

Serotonin is used to treat what?

A

Selective serotonin reuptake inhibitors (SSRIs) are antidepressants

Triptans (selective 5HT agonists) used for the treatment of migraine

73
Q

Noradrenaline is used to treat what?

A

Reuptake blockers such as tricyclic drugs are antidepressants

MAO inhibitors are antidepressants

Nervous System (40 decks)

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