L11 Peripheral Nervous System

Question 1

What does the nervous system allow the organism to do?

Answer 1

• to sense information about its enviroment
• to respond rapidly and accordingly

Question 2

What are the steps between the input stimulus and the output response?

Answer 2

Detected sensory neurones (PNS and afferent) -> integrated & processed interneurons(CNS) -> effect muscles/glands (PNS and efferent)

Question 3

What are PNS efferent systems?

Answer 3

The autonomic nervous system which controls the smooth muscle and glands
- heart rate, respiratory rate, GI secretions (outside the influence of voluntary control)
- divided into sympathetic and parasympathetic

Somatic nervous system which controls the motor innervation of skeletal muscles
- voluntary control

Question 4

List the characteristics of the sympathetic system

Answer 4

Pupils dilate
Lens of eye adjusts for vision
Airways in lungs dilate
Respiratory rate increases
Heart rate increases
Blood vessels to limb muscles dilate
Blood vessels to visceral organs constrict
Salivary secretions reduced
Brain activity general altertness

Question 5

List the characteristics of the parasympathetic system

Answer 5

Pupils constrict
Lens of eye readjust for closer vision
Airways in lungs constrict
Respiratory rate decrease
Heart rate decrease
Blood vessels to limb muscles constrict
Blood vessels to visceral organs more dilated
Salivary secretions normalise

Question 6

Which neurotransmitters are involved in the sympathetic system?

Answer 6

The preganglionic fibre and the postganglionic fibre join at the synapse
Preganglionic = Ach
Postganglionic = NA

Question 7

Which neurotransmitters are involved in the parasympathetic system?

Answer 7

Preganglionic = Ach
Postganglionic = Ach

Question 8

Which neurotransmitters are involved in the somatic system?

Answer 8

Ach is released onto the neuromuscular junction which is a specialised synapse
Controls the skeletal muscle

Question 9

What are the exceptions in the sympathetic nervous system?

Answer 9

Sweat glands
Both fibres contain Ach

Adrenaline is released from the adrenal glands
- activation of the sympathetic system results in activation of adrenal medulla by Ach which releases adrenaline into the bloodstream

Question 10

What is the precursor choline converted into?

Answer 10

Acetylcholine by cholineacetyl transferase

Question 11

What are the benefits of Ach being stored in vesicles?

Answer 11

• protects it from cytosolic enzymes that can break it down
• available for exocytotic release

Question 12

How is the Ach terminated in the synapse?

Answer 12

Terminated by an enzyme in the synapse = acetylcholinesterase
Ach -> choline + acetate

Question 13

What are the classes of acetylcholine receptors?

Answer 13

1) Muscarinic
2) Nicotinic

Question 14

Outline muscarinic receptors

Answer 14

• located at postganglionic parasympathetic synapses
• 3 main subtypes : M1, 2 and 3
• G-protein coupled recepor

Question 15

Outline nicotinic receptors

Answer 15

2 main receptor subtypes:
Neuronal type - brain and autonomic ganglia (sympathetic and parasympathetic so excitatory)
Muscle type - neuromuscular junction (excitatory)

They have ligand gated ion channels

Question 16

What is the function and structure of G-protein coupled receptors?

Answer 16

S : 7-transmembrane spanning receptors
F : coupled to Intracellular effector systems via a G-protein
Action is slow - seconds

Question 17

What is the function and structure of ligand gated ion channels?

Answer 17

S : made up of 4 or 5 subunits structure
F : coupled directly to an ion channel
Action is very fast - milliseconds

Question 18

Outline muscarinic receptors

Answer 18

M1, 2 and 3
G-protein coupled
Slow response
Mainly located on effector tissues

Question 19

Outline nicotinic receptors

Answer 19

Nic muscle, nic neurone
Ligand gated ion channels
Fast response
Located in ganglia and on NMJ

Question 20

List the effects of muscarinic agonists

Answer 20

Increased pupil constriction
Decreased focal length of the lens
Bronchoconstriction
Decreased cardiac output
Increased GI motility
Increased exocrine gland secretion

They are known as parasympathomimetics as they have similar effects to the activation of the parasympathetic NS

Question 21

What are muscarinic antagonists also known as?

Answer 21

Parasympatholytics as they have opposite effects to the parasympathetic NS

Question 22

What are the clinical uses of muscarinic receptor agonists?

Answer 22

Used to treat glaucoma
- local application causes ciliary muscle contraction
- focuses on near vision and allows increased drainage of aqueous humour
- contraction of sphincter muscle causes pupil constriction

Treatment of dry mouth/reduced saliva secretions
- can result from radiation, antineoplastic drugs, side effects of drugs
- the treatment stimulates saliva secretions and is taken systematically
- side effects include muscarinic-sweating, nausea and minimal cardiovascular side effects

Question 23

What are the clinical uses of muscarinic receptor antagonists?

Answer 23

Pupil dilation in eye surgery
- relaxation of constrictor pupillary muscle

Increased heart rate due to resuscitation in bradycardia

Decrease oral/respiratory secretions before oral procedures and as an adjunct to anaesthesia

Treatment of asthma which relieves bronchodilation

Treats motion sickness
- orally is decreases gastric motility

Question 24

Outline neuronal type nicotinic receptors

Answer 24

located on both sympathetic and parasympathetic ganglia
agonists activate both systems
- sympathetic : vasoconstriction, tachycardia, hypertension
- parasympathetic : bradycardia, hypotension, increased secretions

Question 25

Why are neuronal nicotinic agonists not useful?

Answer 25

Their effect is autonomic confusion

Question 26

What are the characteristics of neuronal type nicotinic receptor antagonists?

Answer 26

Loss of sympathetic and parasympathetic reflexes, especially cardiac

Question 27

Outline muscle type nicotinic receptors

Answer 27

Located at the NMJ
Stimulation of these receptors by Ach causes depolarisation and contraction of the skeletal muscle fibres
- in muscle fibres the depolarisation is known as end plate potential (EPP)

Question 28

What is the effect of a nicotinic agonist on the NMJ?

Answer 28

Initial depolarisation and muscle fibre contraction
- because the synthetic agonist is not metabolised rapidly by acetylcholinesterase
- the fibre is persistently depolarised resulting in loss of further electrical excitability -> depolarising block
- can be used for paralysis/muscle relaxation for surgery

Question 29

What is the effect of nicotinic antagonists at the NMJ?

Answer 29

Hyperpolarisation
Inhibition of EPPs
Muscle fibre relaxation
Paralysis for surgery
Non-depolarising blocker

Question 30

How can drugs affect the synthesis in cholinergic transmission?

Answer 30

Hemicholinium blocks the choline uptake, inhibits synthesis and blocks Ach transmission

Question 31

How can drugs affect the release during cholinergic transmission?

Answer 31

Ach release is inhibited by botulinum toxin and bungarotoxin
- causes parasympathetic and motor paralysis if injected

Botulinum toxin injected locally is used to treat muscle spams and in plastic surgery (BOTOX)

Question 32

What can inhibit acetylcholinesterase?

Answer 32

Anticholinesterases which increases the transmission of Ach

Question 33

What are the effects of anticholinesterase on the autonomic NS?

Answer 33

Increased transmission at parasympathetic postganglionic synapses
- increased secretions
- bradycardia
- hypotension
- pupil constriction

Question 34

What are the effects of anticholinesterase on NMJ?

Answer 34

Increased muscle tension and twitching, at large doses can cause a depolarising block
Used to treat myasthenia gravis