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Semester 3 > Case 9 - Drug Action in the CNS > Flashcards

Case 9 - Drug Action in the CNS Flashcards

1
Q

what are the four things that happen to neurotransmitters

A

synthesised
stored
released
inactivated

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2
Q

what is ChAT

A

specific to cholinergic neurones and is present in neuronal terminal in excess I.e enzyme is not saturated.

is a precursor

transfer acetate ion from acetyl-CoA to choline to form acetylcholine (I think)

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3
Q

where is acetylcholine stored

A

synaptic vesicles in the axonal terminal

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4
Q

Where is acetylcholine released

A

into the synaptic cleft upon the arrival of an action potential and influx

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5
Q

where does acetylcholine bind

A

to postsynaptic receptors

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6
Q

what are the post synaptic receptors

A

muscarinic (M1-M5)
nicotinic

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7
Q

what happens to 40-50% of the choline formed from ACh breakdown

A

is taken up into presynaptic terminal by active, high affinity transporter specific to cholinergic cells

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8
Q

what breaks down acetylcholine

A

AChE (acetylcholine-esterase) breaks down acetylcholine into choline and acetate

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9
Q

what then happens to the choline

A

it is taken back up into pre synaptic terminals

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10
Q

diagram showing acetylcholine reuptake/inactivation

A
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10
Q

diagram showing acetylcholine reuptake/inactivation

A
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11
Q

where do the cholinergic pontomesencephalon neurones project

A

onto the hindbrain, thalamus, hypothalamus and basal forebrain

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12
Q

what are the two groups of cholinergic neurones that the basal forebrain contains

A

medial septal group
nucleus Basilis group

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13
Q

what is activation of acetylcholine terminated by

A

AChE

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14
Q

sequence of events of acetylcholine at the neuromuscular junction

A

the neuromuscular junction is a chemical synapse between a motor neurone and skeletal muscle fibre. communication between these two cells is carried out by acetylcholine

release of acetylcholine is initiated by the arrival of an action potential propagating along the axon of the motor neurone

depolarisation of the nerve endings leads to opening of presynaptic voltage gated Ca2+ channels and transmitter release Ca2+ dependent vesicle exocytosis

postsynaptic ligand gated ion channels on muscle (nicotinic acetylcholine receptors) open and let Na+ ions into the muscle cell, thus causing depolarisation

action potential is then generated on the membrane of skeletal muscle cell, this allows Ca2+ entry into the muscle cell and this leads to muscle contraction

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15
Q

what is myasthenia gravis

A

an autoimmune condition that affects the nerves and muscles

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16
Q

what happens in myasthenia gravis

A

the immune system produces antibodies (proteins) that block or damage muscle acetylcholine receptors, which prevents the muscles contracting

this prevents messages being based from the nerve endings to the muscles, which results in the muscles not contracting (tightening) and becoming weak

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17
Q

which muscles are most commonly affected

A

eye and facial muscles and those that control swallowing

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18
Q

what medications are prescribed for myasthenia gravis

A

pyridostigmine - prevents the breakdown of acetylcholine

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19
Q

what do agonists at dopamine receptors induce

A

psychotic symptoms

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20
Q

which pathways being blocked lea to side effects e.g parkinsonian side effected

A

mesolimbic pathway
mesocortiyal pathway
tuberoinfundibulnar pathway

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21
Q

what is the usual route of pathway 4 and what happens if you are taking an antipsychotic

A

dopamine uuallly inhibits prolactin but if taking an antipsychotic, you are blocking the inhibition and get the hyperprolactiaemia

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22
Q

how is dopamine made

A

tyrosine
L-dopa
dopamine

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23
Q

what is the dynamic target of seizure control in management of epilepsy

A

is achieving balance between factors that influence excitatory postsynaptic potential (EPSP) and those that influence inhibitory postsyantpic potential (IPSP)

24
Q

what factors lead to a seizure

A

EPSPs
Na+ influx
Ca++ currents
paroxysmal depolarisation

25
Q

what leads to control and not a seizure

A

IPSPs
K+ efflux
Cl- influx
pumps
Low pH

26
Q

what two levels does physiological protection against repetitive firing occur via inhibition

A

the cellular level e.g Na+ Chanel inactivation

the network level e.g GABA mediated inhibition

27
Q

what are the four categories of anticonvulsants

A
  1. drugs that inhibit Na+ channels
  2. drugs that inhibit Ca2+ channels
  3. drugs that enhance GABA mediated inhibition
  4. drugs that inhibit glutamate receptors
28
Q

where do calcium ions flow through

A

T-type calcium channels

29
Q

features of drugs that inhibit Na+ channels

A

enhanced Na+ channel inactivation
AEDs that target the sodium channels prevent the return of these channels to the active state by stabilising them in the inactive state

30
Q

features of drugs that inhibit Ca2+ channels

A

reduced current through T type calcium channels
AEDs that inhibit these T calcium channels are particularly useful for controlling absence seizures

high voltage activated channels - involved in neurotransmitter release

31
Q

what are absence seizures

A

brief, sudden lapse of consciousness

32
Q

what is the syntheses of drugs that enhance GABA mediated inhibition mediated by

A

glutamic acid decarboxylase (GAD)

33
Q

where are drugs that enhance GABA mediated inhibition stored

A

GABA is packaged into presynaptic vesicle by a transporter (VGAT)

34
Q

where is GABA released

A

in response to an action potential and the presynaptic elevation of intracellular Ca2+, GABA is released into the synaptic cleft by fusion of GABA containing vesicles with the presynaptive membrane

34
Q

where is GABA released

A

in response to an action potential and the presynaptic elevation of intracellular Ca2+, GABA is released into the synaptic cleft by fusion of GABA containing vesicles with the presynaptic membrane

35
Q

reuptake of GABA:

A

neurones and glia take up GABA via specific GABA transporters (GATS)

36
Q

what are the 4 GATs

A

GAT-1, GAT2, GAT3, GAT4. each with a specific characteristic distribution in the CNS

37
Q

what enzyme metabolises and breaks down GABA

A

GABA-transmaminase (GABA-T)

38
Q

what do GABA receptor agonists do

A

increase inhibition

39
Q

what do GABA reuptake inhibitors do

A

increase inhibition as would stay around for a bit longer

40
Q

what do GABA transaminase inhibitors do

A

increase inhibition

41
Q

what are the two types of glutamate receptors in the brain

A

ionotropic and metabotropic subtypes

42
Q

what are examples of inotropic receptors and what is a features of these receptors

A

AMPA
Kainate
N-methly-D-aspartate (NMDA)

fast neurotransmission

43
Q

what do AMPA and kainite sites do

A

open a channel through the receptor, allowing sodium and small amounts of calcium to enter

44
Q

what does the NMDA site do

A

opens a channel that allows large amounts of calcium to enter along with the sodium ions. this channel is blocked by magnesium in. the resting state (open later on than the others. excitatory signals)

45
Q

what facilitates the opening of the NMDA receptor channel

A

glycine

46
Q

what is the metabotropic site regulated by

A

complex reactions and its response is mediated by second messages

47
Q

what pathway are cocaine and drugs concerned with

A

the dopamine reward pathway with is the mesolimbic pathway

48
Q

what is cocaine and how does it work

A

dopamine reuptake transporter inhibitor.

when cocaine enters the Brain, it blocks the dopamine transporter from pumping dopamine bak into the presynaptic neurone, flooding the synapse with dopamine.

this intensifies and prolongs the stimulation of posynaptic neurones in the brain’s pleasure circuits causing a cocaine high

49
Q

what does methamphetamine do

A

inhibits reuptake transporter but can also increase dopamine production

50
Q

what does nicotine do

A

nicotine receptor is on presynaptic neurone
causing an increase in the release of dopamine
important for feeling of reward pathway

51
Q

what can people who have midl to moderate Alzheimer’s benefit from

A

could benefit from taking a cholinesterase inhibitor.

52
Q

how do cholinesterase inhibitors work

A

by increasing the amount of a chemical called acetylcholine which helps messages travel around the brain. cholinesterase inhibitors do not prevent the disease from progressing but may help people to function at a slightly high level than they wold do without the drug

53
Q

what are the three cholinesterase inhibitors used

A

donepezil (Aricept)
Rivastigmine (Exeton)
Galantamine (Reminyl)

54
Q

what is increased ACh availability important for

A

controlling memory and cognition

55
Q

what do current treatments for AD provide

A

temporary symptomatic benefits without modifying disease process egg donepezil, galantamine

56
Q

what is the new treatment method for AD

A

amyloid, amyloid plaques are the main marker in SD

57
Q

what are the novel approaches to AD include

A

secretase modulators: decrease Abeta42 production
Anti-aggregants: prevent Abeta aggregation
Immunotherapies : clear Abeta deposition

Semester 3 (94 decks)

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