Neuro muscular junction
Neuromuscular
junction
junction between terminal branch of the nerve fiber and
muscle fiber.
¨ The
neuromuscular junction is the point of synaptic contact between axon terminal
of the motor neuron and the muscle fiber it control
¨ Action
potential in the motor neuron cause acetylcholine release into the NMJ
¨ Muscle
contraction follows the delivery of Ach to the muscle fiber
¨ A
single motor unit consists of a motor neuron and all of the muscles fibers it
controls
¨ The smallest
part of the muscle that can contract individually is known as motor unit
Structure
of neuromuscular junction
Ø Synaptic
tough →axon terminal
Ø Synaptic
cleft →is the space between axon terminal and sarcolemma
Ø Subneural
cleft →fold present in muscle fiber
Ø Synaptic
vesicle →presence in axon terminal and its function is to store Ach
Neuromuscular transmission
¨ Defined
as the transfer of information from motor nerve ending to the muscle fiber
through NMJ
¨ Transmission
takes place by following steps:
1.
release of Ach
2.action
of Ach
3.development
of Epp
4.destruction
of Ach
1.Release
of acetylcholine
¨ When
AP reaches to axon terminal, it increases permeability of presynaptic membrane
for ca++ by opening of voltage gated calcium channel
which is +nce in membrane of axon terminal
¨ Calcium
ion enters to axon terminal from ECF
¨ Excess
of ca++ releases the acetylcholine from syanaptic vesicle
through exocytosis as “quanta” or “packets”
¨ The
Ach diffuses across through the presynaptic membrane & enter the synaptic
cleft
2.Action
of acetylcholine
¨ Ach
binds with nicotinic receptor +nce in the post synaptic membrane
¨ It
opens ligand gated channels for sodium
¨ Sodium
ion enter from ECF but potassium cannot release out from muscle because
potassium & ligand gated channel both have negative charge, so there is
excess of sodium ion which produce an electrical potential called Endplate
potential
3.End
plate potential
¨ EPP
is the change in the resting membrane potential when an impulse reaches the
NMJ. The resting membrane potential at the NMJ is -90 mv. When sodium ions
enters inside, slightly depolarization occurs up to -60 mv which is called EPP
¨ The
EPP is not propagative. But it causes the development of APin the muscle fiber
4.Fate
of acetylcholine
¨ Ach
is released into the synaptic cleft is destroyed very quickly.
¨ With
in 1 millisecond after the release into the synaptic cleft, it is destroyed by
the acetylcholinesterase.
¨ However,
the Ach line so potent, that even this short duration of 1 millisecond is sufficient
to excite the muscle fiber
¨ Rapid
destruction of Ach prevents the repeat excitation of the muscle fiber
&allow the muscle to relax
Myasthenia
gravis
¨ Antibodies
to Ach receptor at NMJ
¨ This
block ach receptors of NMJ
¨ Destroys
Ach receptors & triggers endocytosis of Ach receptor.
¨ Neuromuscular
transmission is blocked
¨ Easy
fatigability on exercise
¨ May
lead to paralysis
Lambert-Eaton
syndrome
¨ Condition
that resembles the myasthenia gravis
¨ Rare
condition
¨ Antibodies
to the voltage-gated calcium ion channels on nerves endings
¨ Impaired
release of Ach at NMJ
¨ Proximal
muscles of lower extremities are affected
Hi there,
ReplyDeleteThanks for these notes, but just wondering what is +nce?