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PED1003 pharmacology > central nervous system L14-16 > Flashcards

central nervous system L14-16 Flashcards

1
Q

Parkinsonism

A

drug/stroke/infection induced symptoms

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2
Q

motor symptoms of parkinsons

A

resting tremor
muscle rigidity
suppression of voluntary movements

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3
Q

post-mortem neuropathology of Parkinson’s

A

loss of DA cell bodies in substantia nigra
(PET images)

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4
Q

pathology of Parkinson’s disease

A

degeneration of DAergic neurones of nigrostriatal tract
therefore loss of DA transmission in striatum

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5
Q

parkinsonism pathology

A

any condition in which DA transmission is lost in striatum via D2
pharmacological blockade/ brain lesion

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6
Q

4 dopamine pathways in brain

A

nigrostriatal
mesocortical
mesolimbic
tuberoinfundibular

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7
Q

nigrostriatal

A

substantia nigra to striatum

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8
Q

mesolimbic

A

ventral tegmental area to frontal cortex

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9
Q

tuberoinfundibular

A

arcuate nucleus to pituitary gland

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10
Q

pharmacotherapeutic aim of Parkinson’s

A

increase DA transmission in striatum

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11
Q

dopamine synthesis

A

tyrosine > L-DOPA > dopamine
via tyrosine hydrolase and then DOPA decarboxylase

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12
Q

dopamine storage

A

vesicles
VMAT transports DA to vesicles

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13
Q

dopamine metabolism

A

monoamine oxidase (MAO) will metabolise DA outside the vesicles

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14
Q

DA metabolism process

A

DA > DOPAL > DOPAC > HVA (Homovanillic acid)

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15
Q

monoamine oxidase isoforms

A

MAOa and MAOb
different gene products
both on X chromosome
MAOb mainly metabolises DA

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16
Q

DA release

A

depolarization of terminal causing exocytosis
v-gated Ca2+ channels allow Ca2+ into terminal
vesicles fuse w membrane

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17
Q

DA receptors

A

G-protein coupled
D1-like > stimulate adenylate cyclase/ excitatory
D2-like> stimulate inhibit adenylate cyclase/ open K+channel

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18
Q

DA reuptake

A

via transporter/ DAT

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19
Q

L-DOPA

A

levodopa
precursor bypassing rate-limiting enzyme
^DA synthesis

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20
Q

DA polarity

A

can’t cross membranes
sympathomimetic effects
metabolised in gut by MAO

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21
Q

MAO inhibitor

A

selegiline
MAOb inhibitor
blocks intraneuronal metabolism of DA
^DA content of vesicles
less intraneuronal breakdown

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22
Q

D2 Receptor agonists

A

bromocriptine
or apomorphine/ lisuride
(inhibit striatal output neurones directly)

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23
Q

Parkinson’s therapeutics

A

L-DOPA w carbidopa
given in combo, effects wear off as neurons degenerate
:( psychosis/ cognitive dysfunction/ addiction

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24
Q

latroigenic/ drug-induced parkinsonism

A

antipsychotic drugs block D2 receptors in all 4 pathways

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25
Q

depression symptoms

A

poor concentration
altered appetite
anhedonia
despair

26
Q

depression pathology

A

unknown
pharma suggests dysfunction of 5-HT/NA systems (noradrenaline/ 5-hydroxytoyptamine)

27
Q

locus coerulus

A

NAergic cell bodies projecting to hypothalamus and midbrain/ hippocampus and cortex

28
Q

dorsal and median raphe nuclei

A

contain seretonergic pathways

29
Q

NA production

A

tyrosine> (tyrosine hydroxylase)> L-DOPA> (DOPA decarboxylase)> dopamine> (dopamine beta-hydroxylase)> noradrenaline

30
Q

5-HT production

A

tryptophan> (tryptophan hydroxylase)> 5-HTP> (5-HTP decarboxylase)> 5-HT

31
Q

NA/ 5-HT storage

A

in vesicles protecting from MAO
intraneural metabolism by MAO

32
Q

NA/5-HT metabolism

A

MAO
present in DA/NA/5-HT
transmitter breakdown in cytosol
MAOa and MAOb metabolize both NA/5-HT

33
Q

NA metabolism process

A

NA>(MAO/aldehyde dehydrogenase)> DOPEG>(catechol-o-methyl transferase)> MHPG

34
Q

5-HT metabolism process

A

5-HT>(MAO)>aldehyde>(aldehyde dehydrogenase)> 5-HIAA

35
Q

NA/5-HT release and receptors

A

depolarization causes exocytotic release

36
Q

NA receptors

A

G-protein coupled receptors
alpha/ beta
a1> stimulate P1 cycle
a2> inhibit adenylate cyclase/ open K+ channels/ hyperpolarize/ ^cAMP
B1,2,3> stimulate adenylate cyclase

37
Q

5-HT receptors

A

G-protein coupled
5-HT(a-f) > inhibit adenylate cyclase
5-HT(1a)> open K+ channel
5-HT2(a-c)> stimulate P1 cycle
ligand gated ion channel
5-HT3

38
Q

autoreceptors

A

NA and 5-HT release
inhibit transmitter release
NA>a2
5-HT>5-HT1b

39
Q

5-HT/ NA termination

A

high affin reuptake transporter removes from synaptic cleft
*monoamine reuptake transporters > distinct transporters proteins/ preferentially take up NA/5-HT

40
Q

monoamine theory of depression

A

relative decrease in NA/5-HT neurotransmission underlies depression symptoms

41
Q

present antidepressant targets

A

^NA/5-HT
MAO inhibitors
reuptake inhibitors

42
Q

MAOIs

A

inhibit MAO and intracellular 5-HT/NA metabolism
^ vesicular 5-HT/NA content/ release

43
Q

MAOI effects

A

stimulant ^DA transmission
^sympathomimetic amine actions (“cheese reaction”)
interact w reuptake inhibitors

44
Q

TCA

A

tricyclic antidepressants
H1/ACh/a1 antagonism > postural hypotension/ dry mouth/ sedation
e.g. imipramine/ amitryptiline

45
Q

SSRI’s

A

selective serotonin reuptake inhibitors
inhibit 5-HT reuptake selectively
e.g. prozac, sertraline/zoloft, paroxetine

46
Q

antidepressants delayed therapeutic actions

A

autoreceptor desensitization
synaptic remodelling

47
Q

reward pathway

A

DA neurones w cell bodies in ventral tegmental area projects to n.accumbens> activation releases DA> acts on inhibitory D2 receptors, inhibitting n.accumbens

48
Q

amphetamine mechanism

A
  1. enter nerve terminal via PM transporter
  2. vMAT2 transport
  3. neurotransmitter release into cytosol
  4. membrane transporter reverses neurotrans release in cleft
  5. neurotrans reuptake blocked
49
Q

cocaine mechanism

A
  1. binds to DAT PM transporter
  2. DA reuptake blocked
  3. ^DA duration in cleft
50
Q

opioid mechanism

A

via G-protein coupled receptors (mu/ delta/ k)
mu (gut/ spinal chord/ brain stem) > motility/analgesia/resp depression)
n.accumbens mediates euphoria
depends on route of admin/ relative affinity for receptors

51
Q

heroine

A

more lipophilic than morphine/ converted to morphine/ act on mu receptors

52
Q

heroine mechanism

A
  1. activate mu receptors
  2. DA disinhibited
  3. mu activated/ n.accumbens inhibitted
53
Q

ketamine

A

glutamate neurotransmitter acting on CNS neurones
mediated by excitatory ligand-gated ion channel receptors
blocks NDMA receptors

54
Q

CNS glutamatergic neurones

A

long projection neurones/ principal cells connecting cortex and subcortical structures

55
Q

glutamate NMDA receptor

A

allosteric change opens Na+ channel tetrameric
GluN1/GluN2/GluN3 dimers

56
Q

nicotine

A

activates DA neurones directly/ indirectly w glu inputs
agonist at nicotinic ACh receptors

57
Q

nicotinic receptors

A

pentamer
ligand-gated ion channel
Na+/K+ permeable when open

58
Q

cannabinoid receptors

A

THC interaction w G-protein coupled receptors > CB1/CB2
CB1 (expressed in CNS)
CB2 (expressed in immune tissues)

59
Q

retrograde signalling

A
  1. released neurotrans activates receptor on postsyn neurone
  2. cannabinoid released/ CB1 activated on presyn neurone
  3. neurotrans from presyn neurone decreases
60
Q

THC

A

mimics endocannabinoids and decreases presyn neurotrans release
decreases neurotransmission

61
Q

GABA

A

neurotransmitter for widespread neurones
GABAa/GABAb receptor mediation

62
Q

benzodiazepines receptor complex

A

allosteric change opens Cl- channel
BDZs enhance GABAa

PED1003 pharmacology (6 decks)

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