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PBL SEM 3 > 9 - drug action in the CNS > Flashcards

9 - drug action in the CNS Flashcards

1
Q

what is the input region of a neuron, containing lots of receptors?

A

dendrites

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2
Q

how are neurotransmitters stored?

A

in synaptic vesicles

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3
Q

what are the 2 methods of inactivation/reuptake of neurotransmitters?

A
  1. transporters in presynaptic terminal
  2. enzymes break down neurotransmitter
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4
Q

describe the steps in the release of a neurotransmitter, its action and recycling

A
  1. when an AP arrives at the presynaptic terminal it causes the opening of voltage gated Ca++ channels and Ca++ enters the cell
  2. Ca++ causes the vesicles to bind to the presynaptic membrane
  3. neurotransmitter is released into the synapse by exocytosis
  4. the neurotransmitter binds to receptors on the postsynaptic membrane. the receptor determines if an excitatory or inhibitory signal is passed on
  5. the neurotransmitter is then broken down or directly taken back up into the presynaptic terminal by transporters where it is recycled
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5
Q

what are the precursors of acetylcholine (ACh)?

A

choline + acetyl coenzyme A

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6
Q

describe the synthesis of ACh

A

choline + Acetyl coenzyme A —> coenzyme A + acetylcholine (ACh)

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7
Q

what enzyme is used in the synthesis of ACh?

A

choline acetyltransferase (ChAT)

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8
Q

what does ChAT do?

A

transfers acetate ion from acetyl-CoA to choline

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9
Q

what is special about ChAT?

A
  • specific to cholinergic neurons
  • present in neuronal terminal in excess (ie. enzyme is not saturated)
    ie. with enough precursor you can always make more ACh
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10
Q

how is ACh stored?

A

in synaptic vesicles in the axonal terminal

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11
Q

how is ACh released?

A
  • released into the synaptic cleft upon the arrival of an AP and influx of Ca++

( synaptic vesicles bind with the presynaptic membrane and push the transmitter out into the cleft )

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12
Q

what does ACh bind to?

A

postsynaptic receptors on postsynaptic neuron or muscle — muscarinic (M1-M5) and nicotinic

produces either an inhibitory or excitatory signal

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13
Q

what enzyme is responsible for the breakdown of ACh and what is it broken down into?

A

Acetylcholinesterase (AChE)

breaks down ACh into choline + acetate molecule

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14
Q

once ACh has been broken down, what is taken back up into the presynaptic terminal?

A

choline

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15
Q

what is responsible for the reuptake of choline?

A

choline transporter

choline is recycled and made into ACh — stored in vesicles

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16
Q

the basal forebrain contains what 2 groups of cholinergic neurons?

A
  1. medial septal group
  2. nucleus basalis group
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17
Q

the cholinergic pontomesencephalon neurons project onto what?

A

hindbrain, thalamus, hypothalamus and basal forebrain

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18
Q

what is a neuromuscular junction (NMJ)?

A

a chemical synapse between a motor neurone and skeletal muscle fibre

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19
Q

communication at a NMJ is carried out by what?

A

ACh

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20
Q

what initiates the release of ACh at a NMJ?

A

the arrival of an AO propagating along the axon of the motor neuron

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21
Q

______ of the nerve endings leads to opening of presynaptic voltage-gated ___ channels and transmitter release ___-dependent vesicle _____

A
  • depolarisation
  • Ca++
  • Ca++- dependent
  • exocytosis
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22
Q

how does ACh binding at a receptor in a NMJ lead to depolarisation?

A

postsynaptic ligand-gated ion channels (“nicotinic” ACh receptors) open (conformational change) and let Na+ ions into the muscle cell, thus causing depolarisation

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23
Q

what happens after depolarisation in a muscle cell due to ACh?

A

AP is generated on the membrane of the skeletal muscle cell (due to depolarisation from Na+ entry) — this allows Ca++ entry — muscle contraction

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24
Q

____ entry into the muscle cell leads to muscle contraction

A

Ca++

25
Q

action of ACh is terminated by what?

A

AChE = acetylcholine esterase

26
Q

name a disorder of the NMJ

A

myasthenia gravis

27
Q

describe myasthenia gravis

A
  • an autoimmune condition that affects the nerves and muscles
  • the immune system produces antibodies that block or damage muscle ACh receptors — prevents the muscles contracting (nowhere for ACh to act)
  • this prevents messages being passed from the nerve endings to the muscles — results in the muscles not contracting (tightening) and becoming weak
28
Q

what are commonly affected in myasthenia gravis

A

the eye and facial muscles and those that control swallowing

29
Q

what can be prescribed for myasthenia gravis? how do they work? when do they work best?

A

medications such as Pyridostigmine — inhibitor of AChE — prevent the breakdown of ACh — increase synaptic availability of ACh

these medicines tend to work best in cases of mild myasthenia gravis. they can improve muscle contractions and strength in the affected muscles

30
Q

in schizophrenia where do each of the following symptoms come from in the brain?

  • aggressive
  • affective
  • positive
  • negative
  • cognitive
A
  • aggressive = orbitofrotnal cortex + amygdala
  • affective = ventromedial prefrontal cortex
  • positive = striatum
  • negative = mesocortical/prefrontal cortex, nucleus accumbens reward circuits
  • cognitive = dorsolateral prefrontal cortex
31
Q

antipsychotics working in the dorsal striatum can cause what SE?

A

extrapydramidal symptoms — parkinsonism

32
Q

what does D2 normally do in the tuberoinfundibular pathway?

A

inhibit prolactin release

33
Q

seizure control in management of epilepsy is achieved by what?

A

getting a balance between factors that influence excitatory postsynaptic potential (EPSP) and those that influence inhibitory postsynaptic potential (IPSP)

too much excitation = SEIZURES

34
Q

what excitatory and inhibitory factors need to be in balance in treating epilepsy?

A

excitatory:
- EPSPs
- Na+ influx
- Ca++ currents
- paroxysmal depolarisation

inhibitory:
- IPSPs
- K+ efflux
- Cl- influx
- pumps
- low pH

35
Q

what 4 types of drugs are currently available anticonvulsants in epilepsy treatment?

A
  1. drugs that inhibit Na+ channels
  2. drugs that inhibit calcium channels
  3. drugs that enhance GABA-mediated inhibition
  4. drugs that inhibit glutamate receptors
36
Q

explain drugs that inhibit Na+ channels in epilepsy

A
  • prevent the return of Na+ channels to the active state by stabilising the in the inactive state

(normally Na+ depolarises the cell causing AP generation and thus excitation — this is prevented)

37
Q

explain drugs that inhibit Ca++ channels in epilepsy

A
  • calcium channels are important in regulating neurotransmitter release
  • inhibiting these results in reduced current though the T-Type calcium channels
  • stops neurotransmitter release
38
Q

what are calcium channel inhibitors particularly useful in controlling?

A

absence seizures

39
Q

what are high voltage activated channels involved in?

A

neurotransmitter release

40
Q

explain drug that enhance GABA-mediated inhibiton in epilepsy

A
  • GABA receptor agonists — activate GABAR
  • GABA reuptake inhibitors — increase synaptic GABA
  • GABA transaminase inhibitors — reduce breakdown of GABA
41
Q

what mediates the synthesis of GABA?

A

glutamic acid decarboxylase (GAD)

42
Q

how is GABA stored?

A

packed into presynaptic vesicles by a transporter (VGAT)

43
Q

GABA is released into the synaptic cleft in response to what?

A

an AP and the presynaptic elevation of intracellular Ca++

44
Q

how is GABA released into the synaptic cleft?

A

by fusion of GABA-containing vesicles with the presynaptic membrane

45
Q

neurons and glia take up GABA via specific GABA transporters (GATs) — what 4 have been identified?

A

GAT-1, GAT-2, GAT-3 and GAT-4 — each have a characteristic distribution in the CNS

46
Q

how is GABA broken down within cells?

A

metabolised by the widely distributed mitochondrial enzyme GABA-transaminase (GABA-T)

47
Q

what are the ionotropic glutamate receptors?

A

AMPA, Kainate & N -methyl-D-aspartate (NMDA)

48
Q

AMPA + Kainate vs NMDA

A
  • AMPA + Kainate — these sites open a channel throguh the receptor, allowing Na+ and small amounts of calcium to enter. fast acting — important in FAST Glu transmission
  • NMDA — this site opens a channel that allows large amounts of calcium to enter along with the sodium ions. open later than AMDA
49
Q

what is the NMDA channel blocked by in the result state?

A

magnesium

50
Q

what site facilities the opening of the NMDA receptor channel?

A

glycine site

51
Q

the metatropic Glu site is regulated by complex reactions and its response is mediated by ______?

A

second messengers

52
Q

explain drugs that inhibit glutamate receptors in epilepsy

A

inhibit the action of glutamate = less excitation

53
Q

where do CNS stimulants (drugs of abuse) have their main effect?

A

mesolimbic pathway:
ventral tegmental area (VTA : A10) in midbrain to limbic regions associated with reward, motivation, affect and memory
—> reward pathway

54
Q

what does cocaine do?

A

inhibits DA transporter — inhibits reuptake — increases synaptic DA — intensifies and prolongs the stimulation of postsynaptic neurons in the brains pleasure circuits, causing a cocaine “high”

55
Q

how does methamphetamine work?

A

increases release and inhibits transporter of DA

56
Q

how does nicotine work?

A

activates presynaptic receptors — increases DA release in reward pathway

57
Q

what are the current treatments for Alzheimer’s disease?

A

cholinesterase inhibitor — prevents ACh breakdown — increase ACh in synapse = good for cognition

they restore symptoms but don’t prevent degeneration of ACh neurons (cause)

58
Q

what are some novel approaches to treating Alzheimer’s?

A
  • secretase modulators — decrease AB42 production
  • anti-aggregants — prevent AB aggregation
  • immunotherapies — clear AB deposition

prevent amyloid buildup and neuroinflammation

59
Q

what is AB in alzheimer’s?

A

AB peptide is precursor to amyloid plaques seen in AD

— AB deposition and neurodegeneration

PBL SEM 3 (49 decks)

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