L11 Peripheral Nervous System Flashcards
What does the nervous system allow the organism to do?
- to sense information about its enviroment
- to respond rapidly and accordingly
What are the steps between the input stimulus and the output response?
Detected sensory neurones (PNS and afferent) -> integrated & processed interneurons(CNS) -> effect muscles/glands (PNS and efferent)
What are PNS efferent systems?
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
List the characteristics of the sympathetic system
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
List the characteristics of the parasympathetic system
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
Which neurotransmitters are involved in the sympathetic system?
The preganglionic fibre and the postganglionic fibre join at the synapse
Preganglionic = Ach
Postganglionic = NA
Which neurotransmitters are involved in the parasympathetic system?
Preganglionic = Ach
Postganglionic = Ach
Which neurotransmitters are involved in the somatic system?
Ach is released onto the neuromuscular junction which is a specialised synapse
Controls the skeletal muscle
What are the exceptions in the sympathetic nervous system?
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
What is the precursor choline converted into?
Acetylcholine by cholineacetyl transferase
What are the benefits of Ach being stored in vesicles?
- protects it from cytosolic enzymes that can break it down
- available for exocytotic release
How is the Ach terminated in the synapse?
Terminated by an enzyme in the synapse = acetylcholinesterase
Ach -> choline + acetate
What are the classes of acetylcholine receptors?
1) Muscarinic
2) Nicotinic
Outline muscarinic receptors
- located at postganglionic parasympathetic synapses
- 3 main subtypes : M1, 2 and 3
- G-protein coupled recepor
Outline nicotinic receptors
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
What is the function and structure of G-protein coupled receptors?
S : 7-transmembrane spanning receptors
F : coupled to Intracellular effector systems via a G-protein
Action is slow - seconds
What is the function and structure of ligand gated ion channels?
S : made up of 4 or 5 subunits structure
F : coupled directly to an ion channel
Action is very fast - milliseconds
Outline muscarinic receptors
M1, 2 and 3
G-protein coupled
Slow response
Mainly located on effector tissues
Outline nicotinic receptors
Nic muscle, nic neurone
Ligand gated ion channels
Fast response
Located in ganglia and on NMJ
List the effects of muscarinic agonists
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
What are muscarinic antagonists also known as?
Parasympatholytics as they have opposite effects to the parasympathetic NS
What are the clinical uses of muscarinic receptor agonists?
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
What are the clinical uses of muscarinic receptor antagonists?
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
Outline neuronal type nicotinic receptors
located on both sympathetic and parasympathetic ganglia
agonists activate both systems
- sympathetic : vasoconstriction, tachycardia, hypertension
- parasympathetic : bradycardia, hypotension, increased secretions
Why are neuronal nicotinic agonists not useful?
Their effect is autonomic confusion
What are the characteristics of neuronal type nicotinic receptor antagonists?
Loss of sympathetic and parasympathetic reflexes, especially cardiac
Outline muscle type nicotinic receptors
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)
What is the effect of a nicotinic agonist on the NMJ?
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
What is the effect of nicotinic antagonists at the NMJ?
Hyperpolarisation
Inhibition of EPPs
Muscle fibre relaxation
Paralysis for surgery
Non-depolarising blocker
How can drugs affect the synthesis in cholinergic transmission?
Hemicholinium blocks the choline uptake, inhibits synthesis and blocks Ach transmission
How can drugs affect the release during cholinergic transmission?
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)
What can inhibit acetylcholinesterase?
Anticholinesterases which increases the transmission of Ach
What are the effects of anticholinesterase on the autonomic NS?
Increased transmission at parasympathetic postganglionic synapses
- increased secretions
- bradycardia
- hypotension
- pupil constriction
What are the effects of anticholinesterase on NMJ?
Increased muscle tension and twitching, at large doses can cause a depolarising block
Used to treat myasthenia gravis
