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Francesca's ESA2 > M&R 10.1/10.2 The ANS > Flashcards

M&R 10.1/10.2 The ANS Flashcards

1
Q

The ANS is entirely afferent/efferent but is regulated by afferent/efferent inputs

A

The ANS is entirely EFFERENT, but is regulated by AFFERENT inputs

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2
Q

Generally in the ANS, are preganglionic fibres myelinated or unmyelinated?

A

Myelinated

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3
Q

Generally in the ANS, are post-ganglionic fibres myelinated or unmyelinated?

A

Unmyelinated

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4
Q

Where is the origin of the parasympathetic nerves?

A

Craniosacral

Lateral horn of medulla (cranial nerves 3,7,9,10)
Sacral region of spinal cord

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5
Q

Describe the preganglionic and post-ganglionic fibres in the PNS, and the location of the ganglia

A

Preganglionic fibres - Long & myelinated

Ganglia in the tissue innervated by the post-ganglionic fibres

Post-ganglionic fibres - short and unmyelinated

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6
Q

Describe the origin of the sympathetic nerves

A

Thoracolumbar

From lateral horn of lumbar and thoracic spinal cord

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7
Q

Describe the preganglionic and post-ganglionic fibres in the sympathetic NS and the location of the ganglia

A

Pre-ganglionic fibres = Short & myelinated

Ganglia - in the paravertebral chain (close to the spinal cord)

Pos-ganglionic fibres = long and unmyelinated

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8
Q

All preganglionic neurons in the ANS use what as their neurotransmitter? What post-ganglionic receptors does it act on?

A

Acetylcholine

Nicotinic receptors (nAChRs - ligand-gated ion channels)

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9
Q

In the parasympathetic NS, postganglionic neurons release what as their neurotransmitter? What receptors does it act on in the target tissue?

A

Acetylcholine

Muscarinic receptors (mAChRs - [GPCRs])

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10
Q

In the sympathetic NS, what neurotransmitter do MOST post-ganglionic neurons release? What receptors does it act on in the target tissues?

A

Noradrenaline (NA)

Adrenoceptors (alpha1, alpha2, beta1, beta2, beta3) - GPCRs

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11
Q

Which post-ganglionic neurones in the sympathetic NS do not release noradrenaline?
What do they release instead? What receptors does it act on?

A

Those innervating sweat glands and hair follicles (for piloerection)

They release acetylcholine, which acts on muscarinic receptors (mAChRs)

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12
Q

In the sympathetic NS, what are chromaffin cells and what can they be considered as? What do they do?

A

They are neurosecretory cells in the adrenal glands (adrenal medulla)
They can be considered as post-ganglionic sympathetic neurons that don’t project to a target tissue
Instead they release ADRENALINE into the BLOODSTREAM

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13
Q

In the ANS, what are NANC transmitters? When might they be released?

A

Non-adrenergic , non-cholinergic transmitters

They can be co-released with either NA or ACh

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14
Q

Name some NANC transmitters found in the ANS

A

ATP
NO
5-HT (serotonin)
Neuropeptides (e.g. VIP and substance P)

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15
Q

What are the effects of PNS innervation on the heart?

Via which receptors?

A

Negative choronotropy (bradycardia)

Via ACh acting on M2 receptors in the SAN (and in AVN -to reduce conduction velocity)

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16
Q

What are the effects of PNS innervation on the bronchioles?

Via which receptors?

A

Bronchoconstriction

Via ACh acting at M3 receptors in lungs

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17
Q

What is the effect of PNS stimulation on the GIT?

Via which receptors?

A

Increased intestinal motility/secretion

Via ACh acting at M3 receptors in the GIT

18
Q

Generally, where are M1 receptors found and what are their main effects?

A

Neural tissue - autonomic ganglia and cerebral cortex (cause CNS excitation)

(some glands)

19
Q

Generally, where are M2 receptors found and what are their main effects?

A

Cardiac tissue
- atria of heart (cardiac inhibition - negative chronotropy)

(also in CNS)

20
Q

Generally, where are M3 receptors found and what are their main effects?

A

Glandular tissue/smooth muscle

E.g. Exocrine glands (gastric, salivary etc) - increase secretions 
Smooth muscle (e.g. GIT, eye, airways, bladder) - constriction
Blood vessels (endothelium) - vasodilation
21
Q

Generally, where are alpha1 adrenoceptors found and what are their main effects?

A

Smooth muscle

  • > Blood vessels & bronchi - CONSTRICTION
  • > GIT smooth muscle - RELAXATION
  • > GI sphincters, uterus, bladder sphincter, seminal tract, radial muscle of iris- CONTRACT

Liver - glycogenolysis

22
Q

Generally, where are alpha2 adrenoceptors found and what are their main effects?

A

Pancreatic islets - decrease insulin secretion

Blood vessel SM - constrict/dilate
GIT SM - relax

23
Q

Generally, where are beta1 adrenoceptors found and what are their main effects?

A

Heart

  • > Increase HR (positive chronotropy)
  • > increase force of contraction (positive inotropy)
24
Q

Generally, where are beta2 adrenoceptors found and what are their main effects?

A

Smooth muscle

  • > blood vessels & bronchi - DILATE
  • > GIT, uterus, bladder detrusor, seminal tract & ciliary muscle - RELAX

Skeletal muscle

  • > increased muscle mass & speed of contraction
  • > glycogenolysis

Liver - glycogenolysis

25
Q

Generally where are beta3 adrenoceptors found and what do they do?

A

Skeletal muscle - thermogenesis

Fat - lipolysis, thermogenesis

26
Q

What do sensory inputs to the ANS do?

A

Monitor:
Levels of CO2, O2 & nutrients in blood
Arterial pressure
GIT content & chemical composition

27
Q

Where do the primary sensory neurons of the ANS project? What does this form?

A

onto ‘second order’ sensory neurons in the medulla oblongata

Forms the nucleus tractus solitarius (nTS) that integrates all visceral afferent information

28
Q

What are the main steps in neurotransmission (from nerve terminal to receptor)?

A
  1. Uptake of precursors 2. Synthesis of NT
  2. Vesicular storage of NT 4. Degradation of NT (in terminal)
  3. Depolarisation by AP 6. Influx of Ca2+
  4. Exocytosis of NT 8. Diffusion of NT across cleft
  5. Interaction with post-S receptors 10. Inactivation of transmitter
  6. Reuptake of transmitter 12. Interaction with pre-S receptors
29
Q

Which steps in neurotransmission are the most common sites of drug action?

A
  1. Degradation of NT (in terminal)
  2. Interaction with post-synaptic receptors
  3. Inactivation of NT
  4. Reuptake of NT
  5. Interaction with pre-synaptic receptors
30
Q

How is acetylcholine synthesised? What catalyses this?

A

Acetyl CoA + choline –> acetylcholine + CoA

Catalysed by CAT (cholineacetyltransferase)

31
Q

How is acetylcholine degraded? What catalyses this?

A

Acetylcholine –> acetate + choline

Catalysed by AChE (acetylcholinesterase)

32
Q

How can AChE inhibitors be useful?

A

By enhancing the actions of endogenously released ACh

E.g. pyrostigmine used for myesthenia gravis

33
Q

What is the problem with non-selective mAChR agonists?

How might this be prevented?

A

They will cause autonomic side effects, e.g. decreased heart rate (and therefore decreased CO) , increased bronchoconstriction and GIT peristalsis, increased sweating & salivation

Can be prevented by administering locally - e.g. pilocarpine in glaucoma

34
Q

What happens after NA is exocytosed (Ca2+ dependent) from the synaptic cleft?

A

It diffuses across the cleft and acts on adrenoceptors on the post-synaptic membrane

It also interacts with pre-synaptic adrenoceptors to regulate nerve terminal processes (e.g. NT release)

It is rapidly removed from the cleft by transporter proteins (so only has a limited time to influence receptors)

35
Q

Describe the two processes involved in termination of NA signalling

A

Uptake 1 - NA actions terminated by reuptake into the terminal by an Na+ dependent, high affinity transporter

Uptake 2 - any NA not captures by uptake 1 is taken up by a lower affinity, non-neuronal mechanism

36
Q

Which 2 enzymes can metabolise NA that is within the pre-synaptic terminals (not inside vesicles)?

A

MAO (monoamine oxidase)

COMT

37
Q

How can exocytosis of NA be modulated?

A

Pre-synaptic alpha2-adrenoceptor activation

The G-protein beta-gamma subunit can inhibit VGCCs to reduce Ca2+ influx and therefore reduce NT release

38
Q

How do indirectly acting sympathomimetic agents work in the SNS? What is an example?

A

They are taken up into noradrenergic synapse vesicles
They cause NA to be displaced from vesicles - it can then leak into the cleft

e.g. amphetamines

39
Q

Name some drugs that inhibit uptake 1 of NA into the nerve terminal

A 
Tricyclic antidepressants (e.g. amitriptyline)
Selective NA reuptake inhibitors e.g. reboxitine
40
Q

How are beta2 agonists used in asthma?

A

E.g. salbutamol
Used to revers/oppose bronchoconstriction

Beta2 selectivity important to prevent CVS side effects (positive chronotropy and inotropy via beta1 receptors)

41
Q

How are beta1 antagonists used in hypertension? What are they otherwise known as?

A

Decrease heart rate and force of contraction

Beta blockers (e.g. atenolol, bisoprolol)

Francesca's ESA2 (16 decks)

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