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269 > Cholinergic Signalling > Flashcards

Cholinergic Signalling Flashcards

1
Q

Which diseases are caused by disfunction of cholinergic signalling?

A

AD, myasthenia gravis

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2
Q

Which was the first NT to be identified and when?

A

Ach - 1915

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3
Q

How does acetylcholine act in the neuron?

A

As a neurotransmitter and a neuromodulator at the synapse

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4
Q

Which enzyme synthesises Ach?

A

ChAT ( choline acetyl transferase)

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5
Q

Which enzyme degrades Ach?

A

Acetylcholinesterase

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6
Q

How does Ach affect the somatic system?

A

At muscle causes contraction

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7
Q

How does Ach affect the sympathetic NS?

A

released from preganglionic synapses or from nerve to adrenal medulla, causing the release of epinephrine/norepinephrine

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8
Q

How does Ach affect the parasympathetic NS?

A

Ach as a NT in pre and post ganglionic neurons - feed breed, rest and digest

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9
Q

How is it that Ach can have such different effects in the para and sym. NS?

A

Different receptors

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10
Q

Where are ionotropic Ach receptors involved?

A

preganglionic synapse and skeletal muscle

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11
Q

Where are metabotropic Ach recpetors?

A

Post ganglionic in parasympathetic NS

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12
Q

What is an agonist which mimics Ach for ionotropic receptors?

A

nicotine

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13
Q

Which ions have ionotropic Ach receptors?

A

Na+ , K+, Ca2+

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14
Q

What are the characteristic of ionotropic Ach receptors?

A
  • Short duration – millisecond response
  • 5 SU
  • 5 types of subunit combinations: alpha (1-10), beta (2-5), delta, epsilon and gamma
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15
Q

What allows Ach agonist/antagonist drugs to be specific to certain areas of the nervous system

A

Different receptor type

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16
Q

What is an agonist for metabotropic Ach receptors?

A

Muscarine

17
Q

What is an inverse agonist for metabotropic Ach receptors?

A

Atropine

18
Q

What are the characteristics of the metabotropic Ach receptors?

A
  • GPCRs
  • 7 TM domains
  • Long duration – act through second messengers (seconds)
  • Excitatory or inhibitory
  • Can indirectly activate ion channels
19
Q

Describe the different types of muscarinic Ach receptors

A
  • M1 to M5 types – all in CNS
  • M1 – secretory
  • M2 - cardiac
  • M3 - smooth muscle
20
Q

What is the effect of Ach at the NMJ?

A

Release of Ach at NMJ when activated – causes Na+ influx through Ach receptors to initiate a muscle AP, this causes Ca2+ release and then muscle contraction

21
Q

What is the main symptom of mysasthenia gravis?

A

increased muscle weakness on activity?

22
Q

What is the cause of myasthenia gravis?

A

Auto antibodies against nAchR, muscle-specific kinase (Musk), lipoprotein-related protein 4 (LRP4) and agrin

23
Q

Describe Ach breakdown

A
  • By acetylcholine esterase enzyme
  • Really rapid – highest catalytic rate enzyme known
  • Four subunit composition coupled by a sulphydryl linkage to collagen or Proline Rich Membrane anchor to form symmetric form (PRiMA).
  • Anchored to ECM of synapse so can’t diffuse away
24
Q

What are the similarities between organophosphates and AD?

A
  • Block of activity of acetylcholine esterase
  • Accumulation of Ach in synapse leading to chronic depolarisation
  • Antidote: Pralidoxime – binding couples nerve agent and displaces nerve agent from the binding site
  • Ageing – permanent binding
  • Symptoms: SLUDGEM- salivation, lacrimation, urination, defecation, GI upset, emesis and miosis
25
Q

What is the treatment for organophosphates ?

A

• Treatment:
o Atropine- CNS penetrant, acute relief from parasympathetic activation, acts on muscarinic receptors in the CNS
o Diazepam – Reduces release of Ach from the synapse, anticonvulsant drug, CNS effect
o Pralidoxime – Reactivating agent, peripheral paralysis reversal by re-activating AchE, thus allowing metabolism of Ach. CNS non-penetrant

26
Q

What are hte uses of AchE for disease?

A
  • Myasthenia gravis – Use to prolong Ach in NMJ to improve neuromuscular transmission
  • Alzheimers – AchE inhibitors potentiate Ach synapse levels and thus potentiate cholinergic action e.g. Donepezil, rivastigmine and galantamine are reversible selective inhibitors of AchE, show temporary benefit 12-24 months, do not alter the course of the disease

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