Autonomic Nervous System Flashcards

1
Q

Where are the ganglia found in the sympathetic nervous system?

A

In the paravertebral ganglion chain.

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2
Q

What parts of the spine do the sympathetic nerve fibres derive from?

A

The thoracolumbar region

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3
Q

What are of the spine do the parasympathetic nerve fibres derive from?

A

The cervical and sacral spine.

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4
Q

What part of the each vertebrae of the spine do autonomic fibres derive from?

A

The lateral horn of the medulla.

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5
Q

What is a feature of post-ganglionic fibres?

A

They tend to be Unmyelinated.

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6
Q

State the type of transmission which occurs at preganglionic synapses.

A

This is cholinergenic transmission and the post ganglionic nerve cells have nicotinic acetyl choline receptors.

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7
Q

What are nicotinic acetylcholine receptors?

A

These are ligand gated ion channels.

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8
Q

Describe the nature of a parasympathetic post ganglionic synapse.

A

This will have Muscarinic acetylcholine receptors, and these are linked to G proteins.

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9
Q

Describe a sympathetic post ganglionic synapse.

A

At these, there are adrenoceptors which link to GPCRs. The exception to this is sweat glands which have cholinergenic innervation.

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10
Q

What is a chromaffin cell?

A

This is in the adrenal glands and are innervated by the sympathetic nervous system via nicotinic acetylcholine receptors. When stimulated, they release adrenaline into the blood stream for activation of other sympathetic receptors.

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11
Q

Name some molecules which can be coreleased at nerve terminals.

A

ATP, NO, 5-hydroxyhyptamine, neuropeptides.

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12
Q

What is sludge?

A

This is an acronym for functions of the parasympathetic nervous system: salivation, lacrimation, urination, defaecation, gastrointestinal upset, emesis (vomitting)

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13
Q

What is the action of the parasympathetic nervous system in the heart?

A

It acts on the SA node causing bradycardia, and it acts on the AV node to slow conduction rate.

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14
Q

What is the carotid body?

A

This is a chemoreceptors at the carotid artery bifurcation which relays information to the CNS via the glossopharyngeal nerve.

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15
Q

What leads to chemically induced vomitting?

A

Visceral information is input onto the medulla oblongata, and input from area postiema detects toxins in the blood and spinal fluid.

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16
Q

Explain the release of neurotransmitter into synaptic clefts.

A

Neurotransmitter is synthesised and then packaged into vesicles. On membrane depolarisation, Ca influx occurs which causes exocytosis of these vesicles.

17
Q

What three actions in the synaptic cleft can we target drug actions against?

A

Interaction with receptors, inactivation of neurotransmitter and neurotransmitter reuptake.

18
Q

Explain why is is hard to target acetylcholine receptors.

A

Nicotinic receptors exist in both the sympathetic and parasympathetic nervous system so are not a good target for a specific response. There is some possibility of targeting to muscarinic receptors.

19
Q

What is the action of choline acetyl transferase?

A

Acetyl~coA + choline –> acetylcholine + coA

20
Q

How is acetyl choline degraded in the synaptic cleft?

A

This is by acetylcholine esterase and this produces acetate and choline. Choline is reuptake not for synthesis of acetylcholine again.

21
Q

What is an AChE inhibitor?

A

These block the action of acetylcholine esterase and so there is a more prolonged response because more acetyl choline remains in the synaptic cleft for a longer period of time.

22
Q

Name two AChE inhibitors

A

Donepezil and pyridostigmine

23
Q

What is the problem associated with non-specificity of cholinergic drugs?

A

They tend to cause unwanted side effects by reducing pulse rate, increasing bronchoconstriction and stimulating exocrine glands.

24
Q

What functions are mAChR agonists used for?

A

Pilocarpine/bethanechol are used to treat glaucoma and also stimulate bladder emptying.

25
Q

What is the purpose of varicosities?

A

These are close to effector tissues, and so a coordinated response occurs as many synapses are controlled by the same action.

26
Q

What is released at a varicosity?

A

Noradrenaline is released by a Ca2+ dependant method.

27
Q

What is the pathway for noradrenaline synthesis?

A

Tyrosine - DOPA - Dopamine - Noradrenaline

28
Q

Where do vesicles of NA take this up from?

A

They take up newly synthesised NA as well as Na recycled from the synaptic cleft.

29
Q

What is the fate of NA in the synaptic cleft?

A

It is either reuptake not or it is metabolised

30
Q

What two enzymes metabolise NA in the synaptic cleft?

A

Catechol-O-methyltransferase and monoamine oxidase

31
Q

How is NA reuptaken into presynaptic terminal?

A

NA is reuptaken by a high affinity transporter (which is sodium dependant) and also by a low affinity, non-neuronal mechanism

32
Q

Explain how NA release is controlled by presynaptic GPCRs.

A

On presynaptic terminal is a a1 adrenoceptor which can inhibit the VOCC channel when activated. This activation occurs when there is high NA in synaptic cleft and leads to less exocytosis because this is calcium dependant and the calcium channel has been blocked.

33
Q

What are sympathomimetic agents?

A

These are up taken into NA vesicles, displacing NA which leaks into the synaptic cleft causing action on receptors.

34
Q

What are tricyclic antidepressants?

A

These are nor-adrenaline re-uptake inhibitors, and these exert a major action in the CNS.