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BMS11004 > BMS11004 - WEEK 3 FLIPPED LECTURE > Flashcards

BMS11004 - WEEK 3 FLIPPED LECTURE Flashcards

1
Q

what is acetylcholine made from

A

Acetyl group + choline, via ChAT (enzyme lives in cytoplasm of presynaptic cholinergic neurons)

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2
Q

how is acetylcholine broken down in synaptic cleft, and by what

A

by AchE (acetylcholinesterase), into acetic acid and choline
choline is taken up into presynaptic cell by choline transporters and recycled

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3
Q

what 2 type of receptors does acetylcholine act on

A

ionotropic nicotinic
metabotropic muscarinic

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4
Q

where are nicotinic receptors found, and when opened what do they allow

A

neuromuscular junctions
ACh-gated Na/Ca channels
when open, allows positive currents in, depolarising neurons

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5
Q

where are muscarinic receptors found, and what are they used for

A

in CNS, ANS, used in digestion and HR
5 types of GPCRs
M1,3,5 = excitatory
M2,4 = inhibitory

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6
Q

why are muscarinic receptors more present than nicotinic receptors

A

10-100x more mAChRs, than nAchRs as more important for cholinergic signalling

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7
Q

acetylcholine is a common target for many drugs. how may they impact acetylcholine

A
  1. block release
  2. block Acetylcholinesterase (disrupting Ach breakdown)
  3. activate acetylcholine receptors
  4. block receptors
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8
Q

how many botulinum toxin block release of acetylcholine

A

prevent vesicle fusion by destroying SNARE protein so stop release from motor nerves = stop muscle contraction

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9
Q

how can black widow spider venom (latrotoxin) block release of acetylcholine

A

cause large calcium influx. first increases Ach release at NMJ, then eliminates it = cause paralysis

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10
Q

how does nerve gas block acetylcholinesterase so disrupt break-down of acetylcholine

A

AChE inhibitor messing up signalling of parasympathetic nervous system
too much ACh

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11
Q

how can organophosphate pesticides block acetylcholinesterase so disrupt breakdown of acetylcholine

A

insect main NT is ACh
too much excitation = seizure

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12
Q

how can blocking acetylcholinesterase (so disrupting the break-down of acetylcholine) be used as Alzheimer treatment

A

cholinergic neuron dies in brain, but enhancing remaining cholinergic neuron signalling through extending lifespan alleviates some earlier symptoms

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13
Q

how can nicotine, muscarine, or neonicotinoid pesticides work to activate acetylcholine receptors

A

overactivate Ach receptors and overexcites insect nervous system

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14
Q

how can nicotinic toxins block acetylcholine receptors eg: a-bungarotoxin

A

South-American poison arrow dart, reversible, affects nicotinic receptors

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15
Q

how can atropine be used as an antidote of nerve gas (muscarinic, impacting acetylcholine)

A

dilates pupil, increase HR by ACh being used by autonomic nerve
antagonist for muscarinic receptors

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16
Q

what are monoamine synthesised from

A

amino acids

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17
Q

name 2 types of monoamine

A

catecholamine
serotonin (5-HT)

18
Q

what is serotonin synthesised from

A

tryptophan

19
Q

explain structure of catecholamines, and what they also create

A

functional group “catechol”, part of biological pathway
precursor = tyrosine
create NTs dopamine, norepinepherine, epinepherine

20
Q

where are catecholaminergic neurons found

A

regions of nervous system involved in regulation of movement, mood, attentions, visceral function

21
Q

explain rate-limiting steps of catecholamine synthesis

A

enzyme TH catalyses first step in catecholamine synthesis, so is also rate-limiting
TH activities regualted by signals in axon terminal cytosol = causing end-product inhibition
to make more dopamine, add more L-dopa

22
Q

how are monoamines stored

A

packaged into vesicle by VMAT (vesicular monoamine transporter)

23
Q

how are monoamines metabolised, by what

A

MAO (monoamine oxidase), COMT (catechol-O-methyltransferase) on postsynaptic cells

24
Q

are monoamines all metabotropic or ionotropic

A

metabotropic receptors/GPCRs

25
Q

explain divergence of monoamine receptors and the impact this has

A

different receptors activate different G-protein effectors = same molecule can induce different effect on different cell by activating different signalling molecules
different receptor expressed in different neuron types or brain areas, so allow drug to have a specific effect

26
Q

give example for dopamine receptor

A

D1

27
Q

give examples for epinephrine and norepinephrine receptors

A

adrenergic receptors eg: alpha/beta type (betablockers, block adrenergic receptors)

28
Q

give example for serotonin receptors

A

7 receptors, one is a ligand-gated Na+/K+ channel

29
Q

how do cocaine and amphetamines affect monoamines

A

block reuptake of dopamine and norepinephrine = more dopamine in synaptic cleft

30
Q

how do antipsychotics affect monoamines

A

block dopamine receptors so Parkinson symptom

31
Q

how to tricyclic antidepressants affect monoamines

A

block reuptake of NE + serotonin

32
Q

how do opioid peptides work and what can we use them for

A

bind to opioid receptors (GPCRs), regulate pain and coughing/GI tract

33
Q

how does ATP impact monoamines

A

often co-transmitters of monoamines

34
Q

how do endocannabinoids impact monoamines

A

lipid-soluble so not in vesicle and diffuse into membrane, triggering retrograde signalling (signal pass back from post-pre), binding to GPCR

35
Q

how does nitric oxide impact monoamines

A

diffuse through membrane and act on soluble guanylate cyclases

36
Q

how do dopaminergic neurons control motor control

A

dopaminergic neuron in substantia nigra projects to striatum in midbrain
“nigrostriatal” pathway faciliate initiation of vol move

37
Q

how are dopaminergic neurons involved in parkinsons, and how can we treat this

A

die = motor dysfunction
increase dopamine = TH is rate-limiting for dopamine synthesis. increase L-DOPA
early Parkinsons not all dopaminergic neurons dead yet so enhance functioning via L-Dopa

38
Q

how can MAO-B inhibitors be used to treat Parkinsons

A

MAO destroy dopamine = inhibiting it enhances function of remaining dopaminergic neurons in nigrostriatal pathway

39
Q

explain roles of dopaminergic neurons in reward

A

dopaminergic neurons, in ventral tegmental area project to cortex, limbic system = mediates reward/motivations
intra-cranial self-stimulation of mesolimbic pathway = addiction

40
Q

how is epinepherine (noradrenergics) used as a NT to regulate arousal

A

small number in locus coeruleus, send projection over whole brain so wide effects = impact sleep/wake, attention, arousal, mood, memory, anxiety, pain

41
Q

how do serotonergic neurons regulate sleep/wake and mood

A

live in Raphe nuclei, projects all over brain

BMS11004 (29 decks)

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