1. On all postsynaptic
membranes of the preganglionic and postganglionic junction, cholinergic
(acetylcholine sensitive) receptors are present since all preganglionic axons
release acetylcholine to the postganglionic axons. There are two types of
cholinergic receptors: nicotinic and muscurinic. The nicotinic cause fast
action potential while the latter causes slow. The acetylcholine released binds
predominantly with the nicotinic receptors on the postganglionic axons causing
fast action potential also called fast EXCITORY POST SYNAPTIC POTENTIAL (EPSP).
After the fast EPSP has been fired, the acetylcholine may bind with muscurinic
receptors on the post synaptic membrane to cause slow EPSP or slow INHIBITORY
POST SYNAPTIC POTENTIAL (IPSP).
During EPSP, when ACH
(acetylcholine) binds with cholinergic receptors, the Na and Ca channels open
causing their influx generating an action potential. During IPSP when ACH binds
to muscurinic cholinergic receptors, k channels open causing their efflux
resulting in hyperpolarization.
2.The target organs posses both adrenergic (noradrenaline sensitive receptors) for the
sympathetic response and cholinergic MUSCURINIC receptors for the
parasympathetic response. An exception is the receptors on the sweat glands and
blood vessels of skeletal muscles which posses cholinergic MUSCURINIC receptors
and respond to ACH for SYMPATHETIC response.
Note:
the muscurinic receptors are found on postsynaptic membrane of the
postganglionic axon and the target organs while nicotinic are only found on
post synaptic membrane of the post ganglionic axons.
Atropine
can competitively inhibit muscurinic receptor sensitivity to ACH.
Similarly the axons that release ACH are called
cholinergic fibers and those that release Noradrenaline are called adrenergic
fibers.
There are also 4 types of adrenergic receptors a1 a2,
b1 and b2 and are only present on target organs for sympathetic response. A1 is
also present on the presynaptic membrane of the neuroeffector junction.
All respond to
norepinephrine. A1 and a2 on target organs when stimulated cause excitory functions
while b1 and b2 cause inhibitory functions. The a1 present on presynaptic
membrane is stimulated when there is too much norepinephrine in the synaptic
cleft. It inhibits the production of more norepinephrine into the synaptic
cleft.
All beta receptors cause inhibitory effects (e.g. B2
receptors present on lungs cause bronchodilation) except for the b1 receptors
present on myocardium that cause excitory effects.
Note: norepinephrine has a greater effect on alpha
receptors than beta receptors.
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