Autonomic Nervous System Flashcards

1
Q

What does the autonomic nervous system do?

A

The ANS controls all vegetative (involuntary) functions

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2
Q

Give examples of what is controlled by the ANS?

A

heart rate - blood pressure - GI motility - iris diameter

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3
Q

What are the two divisions of ANS?

A
  1. The sympathetic division

2. The parasympathetic division

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4
Q

What does the sympathetic nervous system respond to and what changes does it bring?

A
The sympathetic nervous system responds to stressful situations
• “fight or flight” response
• heart rate increases 
• force of contraction increases
• blood pressure increases
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5
Q

What does the parasympathetic nervous system control?

A

The parasympathetic nervous system regulates basal

activities (e.g. basal heart rate) - “rest and digest”

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6
Q

Is the ANS efferent or afferent?

A

It is entirely efferent (but is regulated by afferent inputs)

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7
Q

What are the Anatomical divisions of brain stem and spinal cord?

A
M = medullary
C = cranial
T = thoracic
L = lumbar
S = sacral
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8
Q

Which regions of the spinal cord, does the sympathetic system emerge from?

A

In the central regions:

Thoracic and lumbar

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9
Q

Which regions of the CNS, does the parasympathetic system emerge from?

A

The medullary and sacral regions (from the brain stem and lower part of spinal cord)

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10
Q

In both the parasympathetic and sympathetic system, where is the pre-ganglion is cell body found?

A

In the CNS

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11
Q

In both the parasympathetic and sympathetic system, where is the post-ganglion is cell body found?

A

In the PNS

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12
Q

In both the sympathetic and parasympathetic system, which neurone is myelinated and which is unmyelinated?

A

The pre-ganglionic neurone is myelinated and postganglionic neurone is unmyelinated

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13
Q

In the sympathetic system, which neurone is longer?

A

The post-ganglionic neurone

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14
Q

In the parasympathetic system, which neurone is longer?

A

The pre-ganglionic neurone

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15
Q

Where do parasympathetic nerves originate from?

A

Originate in the lateral horn of the medulla [and sacral spinal cord]

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16
Q

Where do sympathetic nerves originate from?

A

Originate in the lateral horn of the lumbar and thoracic spinal cord

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17
Q

In the parasympathetic nerves, where are the ganglia located?

A

Ganglia are located within the innervated tissues

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18
Q

In the sympathetic nerves, where are the ganglia located?

A

Ganglia are located in the paravertebral (sympathetic)chain close to the spinal cord

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19
Q

Which are the principal neurotransmitters in the ANS?

A
  • acetylcholine (ACh)

* noradrenaline (NA) (US name: norepinephrine)

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20
Q

Which neurotransmitter do parasympathetic and sympathetic pre-ganglionic neurones release at the ganglia?

A

ACh

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21
Q

What does the pre-ganglionic release of ACH result in?

A

the activation of post-ganglionic nicotinic ACh receptors which results in influx of Na+ ions that causes depolarisation and carries the impulse forward

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22
Q

What type of receptors are Nicotinic ACh receptors?

A

ligand-gated ion channels

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23
Q

True or false, All pre-ganglionic neurons are cholinergic?

A

True

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24
Q

What type of neurones are Parasympathetic post-ganglionic neurons ?

A

Cholinergic

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25
Q

Which receptors do ACh released by Parasympathetic post-ganglionic neurons act on in the target tissue?

A

muscarinic ACh (mACh) receptors

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26
Q

What type of receptors are muscarinic ACh (mACh) receptors?

A

mACh receptors are G-protein coupled receptors (GPCRs).

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27
Q

How many types of mACh receptor subtypes are there?

A

There are five mACh receptor subtypes (M 1,M2,M3,M4,M5).

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28
Q

What type of neurones are most sympathetic post-ganglionic neurons?

A

Noradrenergic

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29
Q

Which is the principal neurotransmitter released by Most sympathetic post-ganglionic neurons ?

A

noradrenaline (NA)

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30
Q

What are the subdivisions of the α-adrenoceptors and β-adrenoceptors?

A

subdivided into α1 and α2 and β1,β2 and β3 subtypes

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31
Q

Which receptors do noradrenaline (NA) interact with?

A

α-adrenoceptors and β-adrenoceptors

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32
Q

Some specialized sympathetic post-ganglionic neurons are

cholinergic, not noradrenergic. Which are they?

A

those innervating sweat glands, hair follicles (piloerection)

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33
Q

Can transmitters other than NA and ACh be found in the ANS?if so, what are they?

A

Yes, Non-Adrenergic, Non-Cholinergic (NANC) transmitters

34
Q

When are theses other transmitters in the ANS released?

A

They may be co-released with either NA or ACh

35
Q

Give examples of Non-Adrenergic, Non-Cholinergic (NANC) transmitters

A
ATP 
nitric oxide (NO) 
5-hydroxytryptamine (5HT; serotonin) neuropeptides (e.g. VIP (vasoactive intestinal peptide), substance P)
36
Q

What is the third division of the autonomic nervous system?

A

The enteric nervous system

37
Q

What does the enteric nervous system control?

A

Controls the gastrointestinal system

38
Q

How are Sympathetic postganglionic neurons in the

adrenal glands different?

A

• They differentiate to form neurosecretory chromaffin cells
• Chromaffin cells can be considered as postganglionic sympathetic
neurons that do not project to a target tissue
• Instead, on sympathetic stimulation these cells release
adrenaline (US name: epinephrine) into the bloodstream

39
Q

Where are chromaffin cells found?

A

Chromaffin cells are present in the

adrenal medulla

40
Q

What innervates the chromaffin cells?

A

Chromaffin cells are innervated by pre-ganglionic sympathetic neurons

41
Q

Which neurotransmitter is used by the somatic efferent system?

A

Acetylcholine on nicotinic acetylcholine receptors

42
Q

What is the physiological consequence of parasympathetic release of ACh on the heart? Which receptor does it act on?

A

Heart(atria):
M2 muscarinic receptors:
- bradycardia - SA node
- reduced cardiac conduction velocity - AV node

43
Q

What is the physiological consequence of parasympathetic release of ACh on smooth muscle? Which receptor does it act on?

A

Smooth muscle:
M3 muscarinic receptors:
• bronchial/bronchiolar contraction - lungs
• increased intestinal mobility/secretion - GI tract
• bladder contraction (detrusor) and relaxation (trigone/sphincter)- GU tract

nitric oxide generation:
• penile erection - GU tract
• ciliary muscle and iris sphincter contraction - eye

44
Q

What is the physiological consequence of parasympathetic release of ACh on glands? Which receptor does it act on?

A

M1/M1 muscarinic receptors:

• increased sweat/salivary/lacrimal secretion -

45
Q

What is the physiological consequence of sympathetic release of NA on the heart? Which receptor does it act on?

A

Heart (atria/ventricles);
B1 adrenoceptors:
• tachycardia (positive chronotropy) - SA node
• positive inotropy - ventricles

46
Q

What is the physiological consequence of sympathetic release of NA on smooth muscle? Which receptor does it act on?

A

Smooth muscle:
a1, B2:
• arteriolar contraction/venous contraction
(arteriolar relaxation in some vascular beds) - vascularise

B2:
• bronchiolar/intestinal/uterine relaxation - lungs/GI/GU tract
• bladder sphincter contraction - GU tract

A1:
•radial muscle contraction - eye

47
Q

What is the physiological consequence of sympathetic release of NA on glands? Which receptor does it act on?

A

Glandular

• increased (viscous) secretion - salivary

48
Q

What is the physiological consequence of sympathetic release of NA on the kidney? Which receptor does it act on?

A

Kidney
A1:
• renin release

49
Q

What are the basic steps in neurotransmission?

A
  1. uptake of precursors
  2. synthesis of transmitter
  3. vesicular storage of transmitter
  4. degradation of transmitter
  5. depolarization by propagated action potential
  6. depolarization-dependent influx of Ca2+ 4
  7. exocytotic release of transmitter
  8. diffusion to post-synaptic membrane
  9. interaction with post-synaptic receptors
  10. inactivation of transmitter
  11. re-uptake of transmitter
  12. interaction with pre-synaptic receptors
50
Q

How is acetylcholine made?

A

It is made from acetyl coenzyme A and choline by the enzyme choline acetyltransferase

Acetyl CoA + choline —-> acetylcholine + coenzyme A

51
Q

How is acetylcholine degraded?

A

Via acetylcholine esterase (AChE)

Acetylcholine —-> acetate + choline

52
Q

Describe cholinergic transmission

A

• Choline from diet and acetyl CoA is combined to make acetylcholine
• Th acetylcholine is packaged into vesicles
• Upon depolarisation of the membrane, the vesicle fuses with the presynaptic membrane and releases the acetycholine into the synaptic cleft
• The acetycholine has two fates:
1. The acetylcholine will interact with receptors and pass on the signal
2. Acetylcholine is degraded

53
Q

How are we able to produce drugs that only target nicotinic acetylcholine receptors in autonomic ganglia?

A

Nicotinic acetylcholine receptors (nAChRs) at autonomic ganglia and the neuromuscular junction differ in structure.

54
Q

What are drugs that target Nicotinic acetylcholine receptors (nAChRs) at autonomic ganglia called?

A

ganglion-blocking drugs

55
Q

Give an example of a ganglion-blocking drug and when is it used?

A

trimethaphan, which is used in hypertensive emergencies and to produce controlled hypotension during surgery

56
Q

Give an example of a mAChR antagonist. What is it used for?

A

tolterodine, which is used to treat “overactive bladder”

57
Q

Give two examples of AChE inhibitors which enhance the actions of ACh. What are they used to treat?

A
  • pyridostigmine*, used to treat myasthenia gravis;

* donepezil*, used to treat Alzheimer’s disease

58
Q

Why are do unwanted side effects often limit the usage of cholinergic drugs?

A

They have a reletive lack of selectivity

59
Q

What side effects could a non-selective, muscarinic ACh receptor agonist cause?

A

Heart rate and cardiac output decreases

In smooth muscle: bronchoconstriction and GI tract peristalsis increases

In exocrine glands: sweating and salivation increases

60
Q

What is the mnemonic for the pathological effects indicative of massive discharge of the parasympathetic nervous system?

A

SLUDGE

61
Q

What does the mnemonic SLUDGE stand for?

A

Salivation: Stimulation of he salivary glands
Lacrimation: Stimulation of the lacrimal glands-tears
Urination:
Defecation
Gastrointestinal upset:
Emesis: Vomiting

62
Q

What usually causes SLUDGE?

A

drug overdose
ingestion of “magic” mushrooms
exposure to organophosphorus insecticides (e.g. parathion),
or nerve gases (e.g. sarin)

63
Q

What do nerve gases do?

A

covalently-modify acetylcholinesterase, to irreversibly deactivate the enzyme and raise acetylcholine levels.

64
Q

What usually causes the symptoms of SLUDGE?

A

The symptoms of SLUDGE are primarily due to chronic (over-)
stimulation of muscarinic acetylcholine receptors, in organs and
muscles innervated by the parasympathetic nervous system.

65
Q

How is SLUDGE treated?

A

SLUDGE may be treated with atropine, pralidoxime, or other anti-cholinergic agents. They are antagonists of muscarinic acetylcholine receptors.

66
Q

When is it useful to use mACh receptor agonists and antagonists?

A

when they can be administered locally, rather than systemically.

67
Q

Give two examples of Muscarinic ACh receptor agonists and what they are used for

A

pilocarpine and bethanechol are respectively used to treat glaucoma and acutely to stimulate bladder emptying.

68
Q

Why are there few side effects of using pilocarpine to treat glaucoma?

A

It can be administered as eye drops so act locally not systemically

69
Q

Give examples of Muscarinic ACh receptor antagonists

A

ipratropium and tiotropium are used to treat some forms of asthma and chronic obstructive pulmonary disease (COPD).
Tolterodine , darifenacin and oxybutynin are used to treat overactive bladder.

70
Q

Describe Post-ganglionic sympathetic neurons

A

Post-ganglionic sympathetic neurons generally possess a highly branching axonal network with numerous varicosities, each of which is a specialized site for Ca2+-dependent noradrenaline release.

71
Q

Describe noradrenaline synthesis

A
  • Tryosine is obtained form the diet
  • Tyrosine is an amino acid that is taken up by the varicosity and conveyed to an intermediate called DOPA
  • The DOPA is converted to dopamine
  • Dopamine is taken up by vesicles that are lined by an enzyme called dopamine B-hydroxylase that convert all of what is taken up into noradrenaline

Within the adrenal medulla noradrenaline is converted to adrenaline by the enzyme (phenylethanolamine N- methyltransferase)

72
Q

What happens following Ca2+-dependent exocytotic release of NA?

A

• NA diffuses across the synaptic cleft and interacts with
adrenoceptors in the post-synaptic membrane to initiate
signalling in the effector tissue
• NA interacts with pre-synaptic adrenoceptors to regulate
processes within the nerve terminal - e.g. NA release

73
Q

Why does noradrenaline only have a very limited time in which to influence pre-
and post-synaptic adrenoceptors?

A

NA has only a very limited time in which to influence pre-and post-synaptic adrenoceptors as it rapidly removed from the synaptic cleft by noradrenaline transporter proteins

74
Q

What happens during (Nor)adrenergic transmission ?

A

• NA actions are terminated by re-uptake into the pre-synaptic
terminal by a Na+-dependent, high affinity transporter
‘Uptake 1’
• NA not re-captured by Uptake 1 is taken up by a lower
affinity, non-neuronal mechanism
‘Uptake 2’

75
Q

Which two enzymes metabolise the noradrenaline within the pre-synaptic terminal that are not taken up into vesicles?

A
  • monoamine oxidase (MAO)

* catechol-O-methyltransferase (COMT)

76
Q

Where in noradrenergic transmission can drugs interfere?

A

In the noradrenaline synthesis
Packaging of noradrenaline
Receptor processes
Reuptake systems

77
Q

What types of drugs are used clinically to target receptors?

A

Subtype-selective adrenoceptor agonists and antagonists are used clinically

78
Q

Give an example of an agonist that is used to target receptors in noradrenergic transmission and what it is used for

A

β-adrenoceptor-selective agonists (e.g. salbutamol) are used
in asthma to reverse/oppose bronchoconstriction

79
Q

Why is β 2-adrenoceptor-selectivity of such agents important?

A

The β 2
-adrenoceptor-selectivity of such agents is
important as it limits possible cardiovascular side-effects (e.g. positive inotropic and positive chronotropic actions)

80
Q

Give an example of an antagonist that is u

A

α1-adrenoceptor-selective antagonists (e.g. doxazosin) and β 1-adrenoceptor-selective antagonists (e.g. atenolol)
are used to treat a number of cardiovascular disorders, including hypertension.