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Science for Medicine > Autonomic and NMJ physiology > Flashcards

Autonomic and NMJ physiology Flashcards

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1
Q

somatic nervous system always sends a signal

A

from spine to Ach to nicotinic receptor straight to target tissue which is always skeletal tissue.
Always gets a response - specialised.

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2
Q

autonomic nervous system:

the sympathetic nervous system always sends signal

A

from spine and has to synapse at the ganglion.
it goes along a Ach and then at ganglion to a nicotinic receptor before reaching the target tissue which is either alpha or beta receptors.
may not always have a response - unspecialised.
preganglionic is short, post ganglionic is long.
neurotransmitters noradrenaline and adrenaline are used.

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3
Q

autonomic nervous system:

the parasympathetic nervous system always sends signals from

A

spine and has to synapse at the ganglion.
it goes along an Ach and then at the ganglion to a nicotinic receptor before reaching the target tissue which has muscarinic receptors.

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4
Q

the autonomic nervous system targets

A

Cardiac muscle
Smooth muscle
GI neurons
Glands

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5
Q

acetylcholine acts on

A

cholinergic receptors:
Nicotinic
- N1 acts on ganglia
- N2 acts on NMJ

Muscarinic

  • M1 acts on neuronal
  • M2 acts on cardiaac and presynaaptic
  • M3 acts on smooth muscle glands
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6
Q

noradrenaline and adrenaline act on

A

adrenergic receptors:
Alpha
A1
A2

Beta
B1 acts on cardiac muscle
B2
B3

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7
Q

cholinergic receptors are either

A

ionotropic
- with integral ion channel and specific ones are selectively activated by nicotine and so are called nicotinic receptors

muscarinic
- selectively activated by muscarine and so called muscarinic

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8
Q

metabotropic receptors are found

A

in adrenergic receptors.

so far no known ionotropic adrenergic receptors.

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9
Q

receptors can be split into groups based on

A
  • what g group they are coupled to

- what secondary messenger signals they produce

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10
Q

steps in synaptic transmission that are common to pretty much all neurotransmitters.

A
  • Transmitter is synthesised and packaged into vesicles.
  • Na+ action potential evokes Ca2+ dependent exocytosis.
  • Triggers Ca2+-dependent exocytosis of pre-packaged vesicles of transmitter
  • Transmitter diffuses across cleft and binds to ionotropic and/or metabotropic receptors to evoke postsynaptic response (on the postsynaptic membrane)
  • Transmitter also binds to presynaptic autoreceptors which inhibit voltage gated Ca2+ channels and curtail further transmitter release.
  • Transmitter is inactivated, usually by uptake into neurones and glia.
  • Transmitter is metabolised, usually, within cells.
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11
Q

Ach is a

A

transmitter

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12
Q

the receptors of ACh are all

A

nicotinic type but differ for ganglionic and NMJ

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13
Q

released ACh is broken down by

A

acetylcholinesterase into acetate and choline.

This is taken back up by neurones and recycled into new ACh to package into vesicles.

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14
Q

how could you stop NMJ synapse working so well

A
  • Inhibit choline transporter (eg hemicholinium)
  • Block voltage gated Ca2+ channels (eg black widow spider venom)
  • Block vesicle fusion (eg botulinium toxins)
  • Use non-depolarising nicotinic receptor blockers (eg d-tubocurarine)
  • Use depolarising nicotinic receptor blockers (eg succinylcholine)
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15
Q

hemicholinium and NMJ

A

Inhibit choline transporter

- blocks some

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16
Q

black widow spider venom and NMJ

A

Block voltage gated Ca2+ channels

- blocks all

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17
Q

botulinium toxins and NMJ

A

Block vesicle fusion

- blocks all unless locally injected

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18
Q

d-tubocurarine and NMJ

A

stop ACh activating the postsynaptic nicotinic receptors by using a competitive antagonist

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19
Q

suxamethoneum and NMJ

A

blocks receptors with an agonist that activates the ion channel and keeps it activated which causes a brief muscle twitching and then paralysis as the voltage gated channels stay in their inactivated (refractory) state.

Has very short lasting action (3-7 minutes)
Twitching stage can cause damage and subsequent pain.

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20
Q

How could you make NMJ synapses work better?

A
  • Prolong the action potential (eg 3,4-aminopyridine)

- Block acetylcholinesterase (eg eserine) so it hangs around in the synaptic cleft for longer

21
Q

how can you prolong action potential using 3,4-aminopyridine?

A
  • let more Ca2+ out and cause more ACh release making Ca2+ action potential longer
  • normally curtailed (restricted) by K+ entering through voltage gated K+ channels (like Na+ release) - blocking then gets more release
22
Q

Clinical applications for NMJ:

Non-depolarising or depolarising blockers used for paralysis during

A
  • surgical procedures
  • electroconvulsive therapy
  • controlling spasms in tetanus
23
Q

Clinical applications for NMJ:

Botulinum toxin used for

A
  • treating muscle spasm

- cosmetic procedures

24
Q

Clinical applications for NMJ:

Anti-cholinesterases used for

A
  • treating myasthenic syndromes
  • reversing action of non-depolarising blockers
  • countering botulinum poisoning
25
Q

Pharmacology of the ANS:

ganglionic transmission - how would you stop transmission

A
  • Inhibit choline transporter (eg hemicholinium)
  • Block voltage gated Ca2+ channels (eg black widow spider venom)
  • Block vesicle fusion (eg botulinium toxins)
  • Block ACh activated channel (eg hexamethoneum)
  • Non-depolarising nicotinic receptor blockers (eg mecylamine)
  • Depolarising nicotinic receptor blockers (eg suxamethoneum)
26
Q

Pharmacology of the ANS:

ganglionic transmission - how would you increase transmission

A

Activate nicotinic receptors (eg nicotine, is more potent at ganglia than NMJ, N1>N2 receptors)

27
Q

Pharmacology of the ANS:

ganglionic transmission - Clinical Applications

A

almost none
- Drugs modulate both sympathetic and parasympathetic ganglionic transmission, and probably NMJ transmission, producing complex actions with many side effects

28
Q

Pharmacology of the ANS:

postganglionic parasympathetic transmission - Clinical Applications

A

Most of the therapeutically drugs target the postsynaptic muscarinic receptors.

  • Muscarinic receptor antagonists (eg atropine)
  • Muscarinic receptor agonists (eg carbachol, pilocarpine)
29
Q

Muscarinic agonists will

A

mimic the effect of the parasympathetic system (ie slow heart rate, contract smooth muscle in airways and bladder, increase gut motility, bronchial secretions and salivation, constrict pupil)

30
Q

Muscarinic antagonists will

A

block effects of the parasympathetic system (ie increase heart rate, relax smooth muscle in airways* and bladder, reduce gut motility, bronchial secretions and salivation, dilate pupil)

31
Q

Relaxing airways and reducing bronchial secretions useful in

A

asthma and anaesthesia,

32
Q

reducing gut hypermotility is useful in

A

irritable bowel syndrome,

33
Q

dilating the pupil is useful in

A

eye examination

34
Q

Pharmacology of the ANS:
postganglionic parasympathetic transmission

Muscarininc agonists (eg pilocarpine) are also used in

A

the treatment of glaucoma - ie high intra occular pressure

35
Q

Pharmacology of the ANS:
postganglionic parasympathetic transmission

Aqueous humour normally

A

drains through the trabecular network into the canal of schlemm

36
Q

Pharmacology of the ANS:
postganglionic parasympathetic transmission

Muscarinic agonists

A

contract the ciliary muscle supporting the lens and contracts the sphincter muscle of the pupil

37
Q

Pharmacology of the ANS:
postganglionic parasympathetic transmission

Glaucoma

A

raises intraoccular pressure.

  • odd one out
38
Q

Pharmacology of the ANS:
postganglionic sympathetic transmission

Block the enzymes that produce

A

NA- noradrenaline (eg carbidopa)

39
Q

Pharmacology of the ANS:
postganglionic sympathetic transmission

Block the transporter that

A

fills the vesicles with NA - noradrenaline (eg reserpine)

40
Q

Pharmacology of the ANS:
postganglionic sympathetic transmission

Introduce a

A

“false” transmitter (eg methyldopa)

41
Q

Pharmacology of the ANS:
postganglionic sympathetic transmission

Activate

A

inhibitory presynaptic (α2) autoreceptors (eg methyldopa)

42
Q

Pharmacology of the ANS:
postganglionic sympathetic transmission

Block

A

α or β postsynaptic receptors (eg doxazosin or propranolol)

43
Q

sympathomimetics

A

potentiate the synapses and make them work better.

can be direct or indirect

44
Q

Pharmacology of the ANS:

postganglionic sympathetic transmission - what makes it work better

A
  • Stimulate NA adrenaline release (eg amphetamine)
  • Inhibit uptake into neurones (eg cocaine & tricyclic antidepressants) or glia (eg phenoxybenzamine)
  • Activate postsynaptic receptors (eg phenylephrine and salbutamol) - direct sympathomimetics
45
Q

α1 agonists used as

A

decongestants and to dilate the pupil (mydriatics)

46
Q

α2 agonists used in

A

the treatment of hypertension

47
Q

Β2 agonists used in

A

treatment of asthma

48
Q

Β1 antagonists used in

A

the treatment of hypertension, angina, cardiac arrhythmias and glaucoma

Science for Medicine (16 decks)

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