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2 - Membranes > deck_762233 > Flashcards

deck_762233 Flashcards

1
Q

Where is acetylcholine released in the nervous sytem?

A

Parasympathetic nervous systema) Pre ganglionic neuronesb) Post ganglionic neuronesSympathetic Nervous Systema) Pre ganglion neuronesb) Some post ganglionic neurones (sweat, ejaculation)

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2
Q

What is acetylcholine synthesized from and how?

A

Choline and Acetyl Co-A, via the action of choline acetyltranferase.

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3
Q

Where does acetylcholine synthesis take place? What enzyme is produced and how does it get to the nerve terminals?

A

Acetycholine synthesized in cholnergic neurones.Choline acetyltransferase made in cell bodies of cholinergic neurones.. Transferred to the nerve terminal by axoplasmic transport.

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4
Q

How is acetylcholine packaged for release?

A

Acetylcholine packed into vesicles and travels to the nerve endings via anteretrograde (movement away from cell body) axoplasmic transport. Stored at nerve ending until action potential arrives.

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5
Q

What is the vesicular ACh transporter?

A

Carrier protein on surface of vesicle in which ACh is absorbed. Actively transport one molecule ACh into vesicle in exchange for two cytoplasmic protons. Example of antiport.

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6
Q

How is ACh released from axon terminal?

A
  • Action potential arrives- Depolarisation causes voltage gates Ca2+ channels to open- Calcium ions diffuse through down their concentration gradient- Ca2+ binds to synaptotagmin - a membrane trafficking protein- Vesicle brought close to membrane- Snare complex makes a fusion pore- Transmitter released through pore
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7
Q

Give an example of an agent which interferes with ACh release

A

Botulinum toxin- Taken into neurones by endocytosis- Has protease activity, cleaves SNARE complex and prevents neurosecretory vesicle from fusing with nerve synapse.

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8
Q

How is acetylcholine degraded?

A

Acetylcholinesterase Abundant enzyme which converts acetylcholine into the inactive metabolies choline and acetate

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9
Q

What happens to the free Choline and Acetate in the synapse?

A

Choline - transported back into the neurone by a high affinity choline transporter on the membraneAcetate- Converted into acetyle CoA and reused to make ACh by choline acetyltransferase

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10
Q

List some of the important sites of parasympathetic innervation

A

Innervation of the heartBronchiolesVasculaturePupil of the eyeEndocrine glands

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11
Q

Wjhat is the effect of increased parasympathetic discharge in the heart?

A

Decrease heart rate (AVN conduction velocity),

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12
Q

Apart from in the parasympathetic system, where else is acetylcholine used in the body?

A

Preganglioncic in the sympathetic nervouse systemPostganglionic in some part of the sympathetic nervous system, notable to sweat glands (M3)

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13
Q

What are two types of acetylcholine receptors?

A

Nicotinic and mucarinic

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14
Q

Why are the two types of acetycholine receptors distinguishable?

A

Muscarinic receptors more sensitive to muscarineNicotinic more responsive to… that’s right, you guessed it! Heroin.Lol, JK. Nicotine.

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15
Q

How do nicotinic acetylcholine receptors cause a post ganglionic response?

A
  • Ligand gated ion channel - Channel permeable to Na+ and K+, causes depolarisation (local, immediate)- Action potential propagatesNicotIONe
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16
Q

How do muscarinic acetylcholine receptors cause a post ganglionic response?

A
  • G-protein coupled receptor- G-protein diffuse to membrane protein- Cascade reaction- Signal propagated to whole of cell- Slow response
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17
Q

What is the class of acetylcholine receptor found at the neuroeffector junction?

A

Muscarinic

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18
Q

For the following sub type, give the G protein, the effector and whether it is activatory or inhibitoryM1

A

GqPhospholipase C activation, creating IP3 that binds to IP3 receptor

19
Q

For the following sub type, give the G protein, the effector and whether it is activatory or inhibitoryM2

A

GiInhibits adenylyl cyclaseOpens potassium channels (decreased firing rate action potentials)Inhibitory

20
Q

For the following sub type, give the G protein, the effector and whether it is activatory or inhibitoryM3

A

GqActivates phospholipase C, creating IP3 that binds to IP3 receptor

21
Q

What is the predominant parasympathetic receptor subtype at the following structures, and give the major physiological actionSA node

A

M2Decreased HR

22
Q

What is the predominant parasympathetic receptor subtype at the following structures, and give the major physiological actionBronchi

A

M3Increased bronchoconstriction

23
Q

What is the predominant parasympathetic receptor subtype at the following structures, and give the major physiological actionBladder

A

M2 & M3 Contraction causing emptying of the bladder

24
Q

What is the predominant parasympathetic receptor subtype at the following structures, and give the major physiological actionGlands

A

M3Increased exocrine and endocrine secretions due to contraction of smooth muscle

25
Q

Parasympathtic nerve terminals at neuroeffector junctions

A

Acts as a negative feedback mechanism to prevent further ACh release from post synaptic vesicles when ACh conc increases in synapse

26
Q

What is a cholinoceptor agonist?q

A

Agent which mimics some or all of the actions of acetycholine

27
Q

What is the advantage of synthesizing a cholinoceptor agonist which oly interacts with a particular receptor subtype?

A

Targeted response can be stimulated

28
Q

What two types of cholinoceptor agonists are available?

A

Direct = Acts as an analogue to stimulate receptors directlyIndirect - Inhibits acetycholinesterase This prevents the breakdown of Ach and therefore prolongs its activity

29
Q

Give an example of a clinical use of cholinoceptor agonist

A

Acelidine - M3 agonistUsed in the treatment of glaucoma, by decreasing intraocular pressure

30
Q

What is a cholinoceptor antagonist?

A

Reduce effects of ACh, can act directly or indirectly with varying levels of selectivity

31
Q

Give an example of Cholinoceptor antagonist and its effects on GI

A

DicyclomineSyptomatic relief of IBS, reduces small bowel symptomsM1 antagonist

32
Q

Why are there so many side effects associated with cholinoceptor antagonists?

A

Control of CNS involves all muscarinic receptors, therefore use of antagonists associated with many side effects

33
Q

How can cholinoceptor antagonists be used as premedication for anasthesia?

A

Atropine - Reduces respiratory secretion, therefore minimies risk of aspiration

34
Q

What effects does the parasympathetic nervous system have on the eye?

A

Causes- Constriction of pupil- Contraction of cillary muscle to the lens, allowing for closer vision

35
Q

What effects does the sympathetic nervous system have on the eye?

A
  • Dilates pupil- Relaxes ciliary muscle, allowing more light to enter the eye and far vision
36
Q

What is glaucoma?

A

Increase in intraocular pressure due to accumulation of fluid

37
Q

What effect does pupil dilation have on glaucoma formation?

A

Impedes drainage of fluid (humour) by blocking the canal of Schlemm

38
Q

What is the most likely cause of glaucoma?

A

DiabetesRaised glucose levels = raised osmosis = increase in intraoccular fluid = compression of optic nerve

39
Q

What are the consequences of increase parasympathetic tone in the eye?

A

Beneficial to glaucoma- Increases constriction of pupil- Causes canal of schlemm to be unblocked- Allows the drainage of extra fluid

40
Q

Which receptor ligands are used to clinically treat glaucoma?

A
  • The sphincter muscle in the eye has M3 muscarinic receptors- Muscarinic agonists will activate contriction of spincter muscles, unblocking drainage path.
41
Q

Givethree non-receptor treatments are used for glaucoma?

A

Protaglandin analogue - increases uveoscleral outflowCarbonic anhydrase inhibitor - decrease aqueous formation by the cillary bodyTopical symathomimetics - reduce intraocular pressure by decreasing aqueous production and increasing aqueous drainage

42
Q

What would be the effects of increasing sympathetic tone of the eye?

A

Dilate the pupilCausing raised intraocular pressure

43
Q

What agents, active at adrenoceptos, are used clinically in the treatment of glaucoma

A

Beta blockers - slow down production of aqueous humour Clonidine - alpha 2- adrenergic agonist - increases uveoscleral outflow

2 - Membranes (24 decks)

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