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10 structure of neuromuscular junction (elctron microscope (underneath…
10
structure of
neuromuscular junction
is the junction betw
the motor neuron
&
skeletal muscle fiber
light microscopic appearence
1.at the termination
the axon loses its myeline sheath
& divides into a no.of
terminal buttons (end feet)
the end feet makes a close contact
with a specialized part of the sarcoplasm
the motor end plate
only 1 nerve fiber ends
on each end plate
elctron microscope
underneath the nerve ending
these folds incr SA on which
NM transmitter can act
the muscle membrane of motor end plate
is thrown into folds called
Palisades
at the terminal nerve endings
there are many
mitochondria &
minute vesicles (synaptic vesicles)/granules
diam 30-50nm
which contain small pkts of the
chemical transmitter A-ch
responsible for synaptic transmission
these vesicles are most numerous at
active zones in the nerve terminal
3.nerve membrane
which is closest to the muscle membrane
is known as the
presynaptic membrane
the space betw these 2 membr is called
the synaptic cleft
(50-100nm) wide which is filled with ECF
the nicotinic Ach receptors
are found on the postsynaptic memb
near the junctional folds
they are so called
cos they are stimulated by both
nicotine & Ach
& inhibited by
curare
enzyme specific 5 acetyl-cholinesterase
an enzyme specific acetyl-cholinesterase
(true or specific cholinesterase)
is found in high conc in
postsynaptic clefts
which destroys (hydrolyses) the Ach
Characteristic features of NM junction
1. easy diffusion
. tip of pallisade
is only 50-100 nm frm preS ending
so diffusion is v easy
( a few hund microsecs)
2.many receptors
an average motor end plate
has abt 50 million
nicotinic receptors
3.releases many Ach molecules
at the same time
when a nerve impulse arrives
it causes almost synchronous release of
approx 106 molecules of Ach
at a single motor nerve ending.
each nerve impulse causes
fusion of 60Ach vesicles
with preS membr
& each vesicle contains
abt 10 molecules of Ach
this amnt is enough to activate
all the nicotinic Ach receptors
4. artificial application of Ach is less effective
than
liberation frm the nerve endings
proof
: when intracellular application of Ach
to the motor end plate by means of
electrophorosis thru a micropipette
10 to the power 8-9 molecules of
Ach are required to depolarise the membr
this also shows that the nicotinic Ach receptors are present on the surface of
motor end plate & not inside the cell
5. fatigue is rare
under normal functioning conditions,
measurable fatigue of NM juction occurs rarely
clinical importance of NM junction
1.blocking of neuromuscular junction
produces muscle relaxation
& so
helps in surgical operations
by providing open fields
reduces movements during
electroconvulsive treatment
of psychotic patients
this blocking can be achieved
in 2 ways
By inhibiting release of Ach
frm preS memb
i.e motor nerve endings
eg: botulinum toxin ( a bacterial toxin)
which combines irreversibly with
cholinergic motor nerve terminals
& interferes with synthesis release of Ach
or
release of A-ch
drugs that antagonize
the action of A-ch
on the postS memb i.e
motor end plate
they act in 2 ways
by competitive inhibition
by persitent depolarization