For movement to occur in our body,

For our body to have a successful
functioning organism, there are many connections made between our nerves and
other parts of our body. In order to do so, one connection happens between
nerves and muscle via nerve cells. The most important for (tiny gap between
nerve cells) are known in-between the spinal motor nerve cell and an extremely
skinny/skeleton-related muscle cellular. Communication is extremely important
for transmission of signal and the muscle because it supports our muscle to be
able to contract or relax. “It is essential for controlling muscle contraction.
NMJ formation requires intimate interactions among motoneurons, muscles, and
SCs” 1 (Stokes, 2017). A neuromuscular junction is a site where
the axons of motor nerves go
to meet the muscle in the body, allowing information to transmit messages from
the brain causing the muscle to contract and relax. The region of the axon is
what processes along skeletal muscle cells. Around these processes are
structures also known as synapses. It is a chemical synapse where the action potential
is in motor neurons. This causes the release of chemical messenger that diffuses
across the gap between the nerve and muscle to initiate contraction.  The motor endplate is known for its specific
structure is the particular synapse made between a spinal neuron and skeletal
muscle cell. For applicable movement to occur in our body, skeletal muscle
contractions are caused by the somatic branch of the nervous system. These
responses quickly to the sensory inputs or descending signals rising in our
brain. The nervous system sends electrical signals, known as action potentials
in the motor neurons, to signal the skeletal muscle cells causing contraction
to occur. “Recll from section 12.8d that varying frequency of action
potentials can also influence the type of neurotransmitter released from the
synaptic knobs for those neurons that store and release more than one type of
transmitter” 2 (McKinely, 2017) . The communication between the
motor neuron and muscle cell is what we called the neuromuscular junction.

 

2.
Activation and anatomical structure of the neuromuscular junction

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The anatomical structure of
the neuromuscular junction is simple in ways that we can understand easier. It consists
of a motor neuron including the motor end plate of a muscle fiber. The related
body structure consists of three kinds of muscle. There are three types that neuromuscular
junction consists of: skeletal muscle, smooth muscle and cardiac muscle. The
skeletal muscle most skeletal muscle is extremely important to connect the
bones in our body. The dominant goal for skeletal muscle is its reduction is extremely
important for aiding and moving the skeleton. Action potentials transfers down
the motor neurons in order to reduce the muscle contraction. Smooth muscle’s
contractions can be spontaneous by the hormones in our body with other chemical
signals controlling it.

Bundles of fibers call
fascicles are founded through a section in skeletal muscle. Myofibrils are
found within these individual muscle fibers that consists of long slender
complex Each of the myofibril is combined of thick and think filaments in order
to arranged in a replicating towards the pattern of their length. These thick
filaments are composed mostly of the myosin. Troponin, tropomyosin and actin
are three proteins that make up the thin filaments. These contain the cyclic
binding between myosin and action of the thick filament and thin filament.
Cross bridge formation is formed when this occurs. This allows the force of
production or allowing the muscle shortening.  Skeletal muscle cell is also consisted in
this structure. Another name for the neuron is also call a spinal motor neuron.
The long processes of neurons are called axons which are located in the motor
neuron. Action potentials are due to ionic mechanisms. There is a voltage
change in Na+ permeability followed by a delayed increase in K+ permeability. This
innervation happens during the process of the axon. The axon enters the
structure of skeletal muscle which consists of branches known as axon
terminals. Synaptic end bulb which are at the end of each axon terminal are the
bulbous. These individual synaptic end blub has synaptic vesicles containing an
important chemical neurotransmitter, also known as acetylcholine. The motor end
plate is located where the muscle fiber part is where the sarcolemma of the
muscle cell.

There are three characteristic features of the junction
synapse. There are two membranes called the pre and post synaptic membranes. Synaptic
cleft is located in the gap in between of presynaptic membrane on the ending of
nerve and the post synaptic membrane on the end plate. Acetylcholine moves from
pre synaptic membrane to the post synaptic membrane by the process of
diffusion. Then there are synaptic vesicles which are sacs filled with air that
present containing neurotransmitter substances. The post synaptic
membrane is present with neurotransmitter receptors that are responsible for
binding the chemical substances. In this structure the neurotransmitter
receptors transmit the signal from the presynaptic neuron. “Each branch of a
motor neuron forms a single junction with a muscle fiber. This is where myelin
sheath locates around the motor axon ends near the surface of the muscle fiber
while the axon divides into a number of short processes that lie embedded in
grooves on the muscle-fiber surface.” 3 (University of Minnesota, 2017).
These Synapses contain Acetylcholine which is the neurotransmitter. The
end-plate potentials can be found at the motor end plate after the presynaptic
membrane is triggered to discharge vesicles containing it.

In the post synaptic
membrane, activity in the motor end plate consists of acetylcholine. They are
gated channels that will eventually become activated by the acetylcholine
leading to the influx of sodium and efflux of potassium. The muscle has a
resting membrane potential of -80mv, but after the influx of sodium the resting
membrane decreases and depolarizes the membrane to 0mv. It depolarizes the
membrane before the opening having the muscle resting membrane potential of
-80mv, but after the influx of sodium the resting membrane potential decreases
from -80mv to 0mv. After this local potential is formed, the end plate
potential occurs.  The miniature end
plate potential consists of a small end plate potential produced by releasing
of Acetylcholine.  This happens so tiny
amounts of sodium influx is presented causing less fluctuation in the resting
membrane potential. In order for the full end plate potential to form, during
the neuromuscular transmission many vesicles are released to form Miniature end
plate potential. The end plate potential takes the resting membrane potential
to a stage of threshold potential. The threshold potential has voltage gated
sodium channels that open causing heavy amount of sodium influx will occur due
to the activation of channels. This will cause the neighboring part of muscle
membrane to the threshold causing it to go under depolarization. In addition,
the wave of depolarization will go to the muscle membrane and in occurrence the
action potential of the neuron will go through the neuromuscular junction as it
reaches the muscle. 

 

3.
Potential Inhibitors

There are different types of potential drugs acting on
neuromuscular junction. One example of this is Hemicholinium. This is a
blockage of accepting choline which will greatly increase the AcH forming cause
it to be reduced. Neurotransmission will not appear when there is not sufficient
amount release of AcH for the generation of action potential.  Many of these toxins occurs within the
inhibitors. Another type of toxin is called Botuliunum Toxin. This is a
proteolytic enzyme that is formed by the aerobic bacteria releasing it as a
type of exotoxin. The toxins then combine within the choline system. During the
nerve ending, they obstruct the control binding of synaptobrevin. A
Neurotransmission blockage would occur when the vesicular membrane is not fused
within the nerve membrane. Another toxin called succinylcholine will lead to an
increase of sodium influx when there it is causing a long stimulation from the
acting receptors. Voltage gated sodium channels are caused by the prolonged
depolarization leading to inactivation of it, also known as depolarizing
neuromuscular blockers. Vesamicole are found within the vesicles and will not
allow the increase of AcH which vesicles come under filled with it. Muscle
weakness would occur if there is less release of AcH and causing a decrease for
neurotransmission to happen. D-Tubcuranin is another toxin that is formed
during the binding controlling by the nicotinic cholinergic receptors
consisting on the post synaptic membrane leading to neurotranissmion to not
happen. It consists of a polarized neuromuscular blockage. In order for the
muscle to relax before the patient is to be operated, the use of general
anesthesia is presented.

 

Acetylcholine (ACh) is synthesized
in motor nerve terminals from the chemical antecedents’ choline and acetyl
coenzyme A. It is facilitated by the enzyme choline acetyl transferase. Slow
leakage of unpackaged ACh from motor nerve terminals can also be detected in skeletal muscle cells. Vesicular
release at the NMJ, as at most other synapses, is the dominant mode of
potential inhibitors
transmitter example. The vesicular acetylcholine supports the acetylcholine to
be transferred into the synaptic vesicles. The vesicular acetylcholine
transporter exchanges ACh for hydrogen ions, which are concentrated within
synaptic vesicles by proton pumps on the vesicular membrane. Both ACh
production and loading of ACh into synaptic vesicles depend (indirectly) on active transport
processes that require energy vesicles in the readily releasable pool tend to
appear ‘docked’ at areas on the presynaptic membrane that are highly
specialized for the
vesicular release of transmitter, called active zones. Active zones are characterized
by high densities of proteins involved in transmitter release, making it possible
to identify active zones on electron micrographs as dark, electron dense
regions of the terminal membrane. In particular, active zones contain high levels of
voltage-gated calcium channels and proteins involved in the fusion of synaptic
vesicles with the terminal
plasma membrane.

 

In the earlier paragraph, I discussed the synapse at the
neuromuscular junction. The synapse has three characteristic features of
chemical synapses in the nervous system. First, there is a discrete separation
between the presynaptic and the post synaptic membrane. The synaptic cleft is
the space between the presynaptic (nerve) and postsynaptic (muscle) membrane. The
space between the two is known as the synaptic cleft. Throughout this space,
signaling mechanism is caused between the presynaptic neuron and the
postsynaptic neuron so that there is information flowing across the synaptic
cleft. Second, synaptic vesicles are contained within the membrane.  The synaptic vesicles contain
neurotransmitter substances that releases ACh then diffuses across the synaptic
cleft causing it to bind to ACh receptors on the skeletal muscle fibre. The synaptic
cleft is the space between the presynaptic (nerve) and postsynaptic (muscle)
membrane. A very thin layer of basal lamina lies within the synaptic cleft and
its lateral extensions bridge the pre- and postsynaptic membranes. The basal lamina
contains numerous factors responsible for the development, maintenance and
regeneration of both of these membranes. Most importantly, the basal lamina contains
the enzyme acetylcholinesterase. This acetylcholinesterase is important because
it terminates synaptic transmission by hydrolysis of ACh into acetate and
choline. AChE is evenly distributed in the basal lamina at a density. When ACh
molecules dissociate from ACh receptors, they diffuse into the synaptic cleft
and bind to AChE, which will once more be available to hydrolyse free ACh, having
already hydrolysed the ACh that was bound to it earlier. The rapid action of
AChE prevents ACh from binding more than once to ACh receptors. The breakdown
of ACh by AChE at the NMJ is a more efficient means of stopping transmission
(and thus muscle contraction) than what occurs at most central nervous system
synapses, where the termination of transmission is most often achieved by the reuptake
of transmitter into the presynaptic terminal. “When the Ach binds to the
receptors, which are made of protein, they open and allow sodium to enter the
cell. This sets off an action potential along the muscle, thus signaling it to
contract” 4 (The Pennsylvania State
University, 2017) .

 

Third is the part that binds the chemical transmitter
substances which has a high density of specialized receptors. This binds the
chemical transmitter substances released from the presynaptic neuron. Acetylcholine
is released from motor nerve terminals and synthesized from choline and acetyl
coenzyme A (acetyl-coA). This motor nerve terminal acts on nicotinic ACh receptors
which are located on a specific area of the skeletal muscle fibres also called the
motor endplate. The ACh receptors are density peaks located near the peaks of
junctional folds. It decreases directly from the NMJ (?10/?m within a few microns from the
synapse). These also contain the folds also known as the voltage-gated sodium
channels. These voltage-gated sodium channels will generate the muscle action
potential allowing it to trigger muscle contraction. By dramatically increasing
the surface area for ACh receptors, it will have a higher possibility to serve
as an increase for the reliability of neuromuscular transmission. This can also
lead to maximizing the effect of synaptic depolarization by segregating ACh
receptors and voltage-gated sodium channels at the crests and depths of it.

 

 

 

 

 

 

 

 

 

Image:             Blackwell,
Wiley. “Negative signals.” Molecular
Control of Neuromuscular Junction. J Cachexia Sarcopenia Muscle. 14 October 2012. 5 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3302983/

 

The stimulation of action voltage
gated is caused by the activity of the sarcolemma and crossing sideways tubule
system causes the stimulation of action voltage-gate channels which is placed
near the tubules. Calcium
is then to be released from the storage site when channels are signaling the
adjacent calcium channels on the sarcoplasmic reticulum, allowing calcium to be
released. The formation of cross bridge between actin and myosin acts on when
intracellular calcium increases (sarcoplasmic concentration) diffuses and binds
to troponin on thin filaments.

 

 

 

4. Conclusion

The primary role of the somatic NMJ in an organism is to
rapidly, reliably and precisely trigger skeletal muscle contraction in response
to action potential firing in a motor neuron. We have described a raft of specializations
at the NMJ that give this synapse its unique response properties. Throughout my
learning in class and research is that the Neuromuscular Junction is an
important for our nerve signals to communicate with our body and initiate the
active of muscles. These specializations include myelination of motor neuron
axons, contributing to their rapid conduction velocity; the large number of
active zones in motor nerve terminals, leading to excess transmitter release;
the rapid termination of ACh binding by AChE, ensuring the temporal fidelity of
transmission, and the clustering of AChRs at the crest of junctional folds in
motor endplates, increasing the likelihood of receptor activation and action
potential firing.

 

“The neuromuscular junction is crucial for life, and they
begin forming early in fetal development…This stimulates the formation of a
muscle specific kinase, which will build receptors for acetylcholine on the
surface of the muscle fiber. This is how the junction is formed, with the
neuron itself emitting the needed chemical for development” 6.  (McMahon, 2017) The binding of
nicotinic receptors on post-synaptic membrane is generated when Neuromuscular
junction is sending signals acetylcholine. The essential binding origin is a
local change in the voltage of the sarcolemma stirring the neighbor channels
causing the K+ to discharge out and Na+ to invade.  The ion act is made up of the action
potential multiplying along the sarcolemma.

The sarcoplasmic reticulum to ryanodine
receptors discharges of calcium because of the increase of voltage gated
channel change beginning of the opening gated dihydropyridine receptors. Cross
bridge formation is then found in between the thick and think filaments. A
component of the contractile apparatus is then cause by the released of calcium
that binds to troponin and increasing a change in tropomyosin. This formation
starts to allow the muscle fiber to shorten and induce the generation of
strength. The cross bridge cycle will continue continuously until the calcium
detaches from troponin. The disconnection of this occurs because calcium discharge
discontinues and it’s effective uptake requires ATP into the sarcoplasmic
reticulum leads to a contraction.