Neuromuscular junction

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Neuromuscular junctions

Electron micrograph showing a cross section through the

neuromuscular junction. T is the axon terminal, M is the
muscle fiber. The arrow shows junctional folds with basal
lamina. Postsynaptic densities are visible on the tips between
the folds. Scale is 0.3 m. Source: NIMH

Detailed view of a neuromuscular junction:

1. Presynaptic terminal
2. Sarcolemma
3. Synaptic vesicle
4. Nicotinic acetylcholine receptor
5. Mitochondrion
Latin synapssis neuromuscularis; junctio neuromuscularis
Code TH H2.00.06.1.02001

The neuromuscular junction connects the nervous system to the muscular system via synapses
between efferent nerve fibers and muscle fibers, also known as muscle cells. As an action
potential reaches the end of a motor neuron, voltage-dependent calcium channels open allowing
calcium to enter the neuron. Calcium binds to sensor proteins on synaptic vesicles called
synaptotagmin triggering vesicle fusion with plasmamembrane and subsequent neurotransmitter
release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release
acetylcholine (ACh), a small molecule neurotransmitter, which diffuses through the synapse and
binds nicotinic acetylcholine receptors (nAChRs) on the plasma membrane of the muscle fiber,
also known as the sarcolemma. nAChRs are ionotropic, meaning they serve as ligand gated ion
channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade
that eventually results in muscle contraction.
Neuromuscular junction diseases can be of genetic and autoimmune origin. Genetic disorders,
such as Duchenne muscular dystrophy, can arise from mutated structural proteins that comprise
the neuromuscular junction, whereas autoimmune diseases, such as myasthenia gravis, occur
when antibodies are produced against nicotinic acetylcholine receptors on the sarcolemma.

Contents

1 Structure
o 1.1 Neuromuscular junction
o 1.2 Acetylcholine receptor

2 Development of the neuromuscular junction

3 Mechanism of action

4 Research methods

5 Toxins
o 5.1 Botulinum toxin
o 5.2 Tetanus Toxin
o 5.3 Snake Venom

6 Diseases
o 6.1 Autoimmune

6.1.1 Myasthenia gravis

6.1.1.1 Neonatal MG

6.1.2 Lambert-Eaton myasthenic syndrome

6.1.3 Neuromyotonia

o 6.2 Genetic

6.2.1 Congenital myasthenic syndromes

6.2.2 Bulbospinal muscular atrophy

6.2.3 Duchenne muscular dystrophy

7 See also

8 External links

9 Further reading

10 References

Structure
Neuromuscular junction
The neuromuscular junction is by definition a synapse, but it differs from synapses between
neurons. Presynaptic motor axons are demyelinated and stop 30 nanometers from the
sarcolemma, the cell membrane of a muscle cell. This 30-nanometer space forms the synaptic
cleft through which signalling molecules are released. The sarcolemma has invaginations called
postjunctional folds, which increase the surface area of the membrane exposed to the synaptic
cleft.[1] These postjunctional folds form what is referred to as the motor end-plate, which possess
acetylcholine receptors (AChRs) at a density of 10,000 receptors/micrometer2 in skeletal muscle.
[2]
The presynaptic axons form bulges called terminal boutons that project into the postjunctional
folds of the sarcolemma. The presynaptic boutons have active zones that contain vesicles,
quanta, full of acetylcholine molecules. These vesicles can fuse with the presynaptic membrane
and release ACh molecules into the synaptic cleft via exocytosis after depolarization.[1] AChRs
are localized opposite the presynaptic terminals by protein scaffolds at the postjunctional folds of
the sarcolemma. Dystrophin, a structural protein, connects the sarcomere, sarcolemma, and
extracellular matrix components. Rapsyn is another protein that docks AChRs and structural
proteins to the cytoskeleton. Also present is the receptor tyrosine kinase protein MuSK, a
signaling protein involved in the development of the neuromuscular junction, which is also held
in place by rapsyn.[1]

Acetylcholine receptor
Acetylcholine is a neurotransmitter synthesized in the human body from dietary choline and
acetyl-CoA (ACoA), and it is involved in the stimulation of vertebrate muscle tissue. The
eukaryotic nicotinic acetylcholine receptor (AChR) is a ligand-gated ion channel. Each subunit
has a characteristic cys-loop, which is composed of a cysteine residue followed by 13 amino
acid residues and another cysteine residue. The two cysteine residues form a disulfide linkage
which results in the cys-loop receptor that is capable of binding acetylcholine and other
ligands. These cys-loop receptors are found only in eukaryotes, but prokaryotes possess ACh
receptors with similar properties.[2] Not all species use a cholinergic neuromuscular junction; in
fact, crayfish have a glutamatergic neuromuscular junction.[1]
AChRs at the skeletal neuromuscular junction form heteropentamers composed of two , one ,
one , and one subunits. When a single ACh ligand binds to one of the subunits of the ACh
receptor it induces a conformational change at the interface with the second AChR subunit.
This conformational change results in the increased affinity of the second subunit for a second
ACh ligand. AChRs therefore exhibit a sigmoidal dissociation curve due to this cooperative
binding .[2] The presence of the inactive, intermediate receptor structure with a single-bound
ligand keeps ACh in the synapse that might otherwise be lost by cholinesterase hydrolysis or
diffusion. The persistence of these ACh ligands in the synapse can cause a prolonged postsynaptic response.[3]
The pre and postsynaptic cells at the neuromuscular junction also contain muscarinic
acetylcholine receptors that are metabotropic receptors coupled with G-proteins. Muscarinic
receptors can be found on the presynaptic cell, which act via negative feedback by binding
acetylcholine molecules and inhibiting the release of more neurotransmitters through a signaling
cascade. G-protein subunits from this receptor can inactivate the calcium channels necessary for
neurotransmitter release. Muscarinic AChRs on the sarcolemma of the postsynaptic cell bind
ACh, which activates a G-protein that opens Kir3.1 potassium channels, thereby hyperpolarizing
the muscle fiber.[1]

Development of the neuromuscular junction

The development of the neuromuscular junction requires signaling from both the motor neuron's
terminal and the muscle cell's central region. During development, muscle cells produce
acetylcholine receptors (AChRs) and express them in the central regions in a process called
prepatterning. Agrin, a heparin proteoglycan, and MuSK kinase are thought to help stabilize the
accumulation of AChR in the central regions of the myocyte. MuSK is a receptor tyrosine kinase
meaning that it induces cellular signaling by binding phosphate molecules to self regions like
tyrosines, and to other targets in the cytoplasm.[4] Upon activation by its ligand agrin, MuSK
signals via two proteins called "Dok-7" and "rapsyn", to induce "clustering" of acetylcholine
receptors.[5] ACh release by developing motor neurons produces postsynaptic potentials in the
muscle cell that positively reinforces the localization and stabilization of the developing
neuromuscular junction.[6]

These findings were demonstrated in part by mouse "knockout" studies. In mice which are
deficient for either agrin or MuSK, the neuromuscular junction does not form. Further, mice
deficient in Dok-7 did not form either acetylcholine receptor clusters or neuromuscular synapses.
[7]

Mechanism of action
See also: Excitation-contraction coupling
The neuromuscular junction is where a neuron activates a muscle to contract. This is a step in the
excitation-contraction coupling of vertebrate skeletal muscle.
1. Upon the arrival of an action potential at the presynaptic neuron terminal, voltagedependent calcium channels open and Ca2+ ions flow from the extracellular fluid into the
presynaptic neuron's cytosol.
2. This influx of Ca2+ causes neurotransmitter-containing vesicles to dock and fuse to the
presynaptic neuron's cell membrane through SNARE proteins.
3. Fusion of the vesicular membrane with the presynaptic cell membrane results in the
emptying of the vesicle's contents (acetylcholine) into the synaptic cleft, a process known
as exocytosis.
4. Acetylcholine diffuses into the synaptic cleft and can bind to the nicotinic acetylcholine
receptors on the motor end plate.
5. These receptors are ligand-gated ion channels, and when they bind acetylcholine, they
open, allowing sodium ions to flow in and potassium ions to flow out of the muscle cell.
6. Because of the differences in electrochemical gradients across the plasma membrane,
more sodium moves in than potassium out, producing a local depolarization of the motor
end plate known as an end-plate potential (EPP).
7. This depolarization spreads across the surface of the muscle fiber and continues the
excitation-contraction coupling to contract the muscle.
8. The action of acetylcholine is terminated when ACh diffuses away from the synapse or
the enzyme acetylcholinesterase degrades part of ACh (producing choline and an acetate
group).
9. The choline produced by the action of acetylcholinesterase is recycled it is
transported, through reuptake, back into the presynaptic terminal where it is used to
synthesize new acetylcholine molecules.[8]

Research methods

Joel del Castillo and Bernard Katz used ionophoresis to determine the location and density of
nicotinic acetylcholine receptors (AChRs) at the neuromuscular junction. With this technique, a
microelectrode was placed inside the motor end-plate of the muscle fiber, and a micropipette
filled with acetylcholine (ACh) is placed directly in front of the endplate in the synaptic cleft. A
positive voltage was applied to the tip of the micropipette, which caused a burst of positively
charged ACh molecules to be released from the pipette. These ligands flowed into the space
representing the synaptic cleft and bound to AChRs. The intracellular microelectrode monitored
the amplitude of the depolarization of the motor end plate in response to ACh binding to
nicotinic (ionotropic) receptors. Katz and del Castillo showed that the amplitude of the
depolarization (excitatory postsynaptic potential) depended on the proximity of the micropipette
releasing the ACh ions to the endplate. The farther the micropipette was from the motor endplate,
the smaller the depolarization was in the muscle fiber. This allowed the researchers to determine
that the nicotinic receptors were localized to the motor end-plate in high density.[1][2]
Toxins are also used to determine the location of acetylcholine receptors at the neuromuscular
junction. -Bungarotoxin is a toxin found in the snake species Bungarus multicinctus that acts as
an ACh antagonist and binds to AChRs irreversibly. By coupling assayable enzymes such as
horseradish peroxidase (HRP) or fluorescent proteins such as green fluorescent protein (GFP) to
the -bungarotoxin, AChRs can be visualized and quantified.[1]

Toxins
Botulinum toxin
Botulinum toxin, (aka. botulinum neurotoxin, BoNT, and sold under the trade name Botox)
inhibits the release of acetylcholine at the neuromuscular junction by interfering with SNARE
proteins.[1] This toxin crosses into the nerve terminal through the process of endocytosis and
subsequently interferes with SNARE proteins, which are necessary for ACh release. By doing so,
it induces a transient paralysis and chemical denervation localized to the striated muscle that it
has affected. The inhibition of the ACh release does not set in until approximately two weeks
after the injection is made. Three months after the inhibition occurs, neuronal activity begins to
regain partial function, and six months, complete neuronal function is regained.[9]

Tetanus Toxin
Tetanus toxin, also known as Tetanospasmin is a potent neurotoxin produced by Clostridium
Tetani and causes the disease state, tetanus. The LD50 of this toxin has been measured to be
approximately 1 ng/kg, making it second only to Botulinum toxin D as the deadliest toxin in the
world. It functions very similarly to botunlinum neurotoxin (BoNT) by attaching and
endocytosing into the presynaptic nerve terminal and interfering with SNARE protein
complexes. It differs from BoNT in a few ways, most apparently in its end state, wherein
tetanospasmin demonstrates a rigid / spastic paralysis as opposed to the flaccid paralysis
demonstrated with BoNT.

Snake Venom

Snake venoms act as toxins at the neuromuscular junction and can induce weakness and
paralysis. Venoms can act as both presynaptic and postsynaptic neurotoxins.[10]
Presynaptic neurotoxins, commonly known as -neurotoxins, affect the presynaptic regions of
the neuromuscular junction. The majority of these neurotoxins act by inhibiting the release of
neurotransmitters, such as acetylcholine, into the synapse between neurons. However, some of
these toxins have also been known to enhance neurotransmitter release. Those that inhibit
neurotransmitter release create a neuromuscular blockade that prevents signaling molecules from
reaching their postsynaptic target receptors. In doing so, the victim of these snake bite suffer
from profound weakness. Such neurotoxins do not respond well to anti-venoms. After one hour
of inoculation of these toxins, including notexin and taipoxin, many of the affected nerve
terminals show signs of irreversible physical damage, leaving them devoid of any synaptic
vesicles.[10]
Postsynaptic neurotoxins, otherwise known as -neurotoxins, act oppositely to the presynaptic
neurotoxins by binding to the postsynaptic acetylcholine receptors. This prevents interaction
between the acetylcholine released by the presynaptic terminal and the receptors on the
postsynaptic cell. In effect, the opening of sodium channels associated with these acetylcholine
receptors is prohibited, resulting in a neuromuscular blockade, similar to the effects seen due to
presynaptic neurotoxins. This causes paralysis in the muscles involved in the affected junctions.
Unlike presynaptic neurotoxins, postsynaptic toxins are more easily affected by anti-venoms,
which accelerate the dissociation of the toxin from the receptors, ultimately causing a reversal of
paralysis. These neurotoxins experimentally and qualitatively aid in the study of acetylcholine
receptor density and turnover, as well as in studies observing the direction of antibodies toward
the affected acetylcholine receptors in patients diagnosed with myasthenia gravis.[10]

Diseases
Any disorder that compromises the synaptic transmission between a motor neuron and a muscle
cell is categorized under the umbrella term of neuromuscular diseases. These disorders can be
inherited or acquired and can vary in their severity and mortality. In general, most of these
disorders tend to be caused by mutations or autoimmune disorders. Autoimmune disorders, in the
case of neuromuscular diseases, tend to be humoral mediated, B cell mediated, and result in an
antibody improperly created against a motor neuron or muscle fiber protein that interferes with
synaptic transmission or signaling.

Autoimmune
Myasthenia gravis
Myasthenia gravis is an autoimmune disorder where the body makes antibodies against either the
acetylcholine receptor (AchR) (in 80% of cases), or against postsynaptic muscle-specific kinase
(MuSK) (010% of cases). In seronegative myasthenia gravis low density lipoprotein receptorrelated protein 4 is targeted by IgG1, which acts as a competitive inhibitor of its ligand,
preventing the ligand from binding its receptor. It is not known if seronegative myasthenia gravis
will respond to standard therapies.[11]

Neonatal MG

Neonatal MG is an autoimmune disorder that affects 1 in 8 children born to mothers who have
been diagnosed with Myasthenia gravis (MG). MG can be transferred from the mother to the
fetus by the movement of AChR antibodies through the placenta. Signs of this disease at birth
include weakness, which responds to anticholinesterase medications, as well as fetal akinesia, or
the lack of fetal movement. This form of the disease is transient, lasting for about three months.
However, in some cases, neonatal MG can lead to other health effects, such as arthrogryposis and
even fetal death. These conditions are thought to be initiated when maternal AChR antibodies are
directed to the fetal AChR and can last until the 33rd week of gestation, when the subunit of
AChR is replaced by the subunit.[12]
Lambert-Eaton myasthenic syndrome
Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder that affects the
presynaptic portion of the neuromuscular junction. This rare disease can be marked by a unique
triad of symptoms: proximal muscle weakness, autonomic dysfunction, and areflexia.[13]
Proximal muscle weakness is a product of pathogenic autoantibodies directed against P/Q-type
voltage-gated calcium channels, which in turn leads to a reduction of acetylcholine release from
motor nerve terminals on the presynaptic cell. Examples of autonomic dysfunction caused by
LEMS includes dry mouth, which is most common, constipation, and erectile dysfunction in
men. Less common dysfunctions include dry eyes and altered perspiration. Areflexia is a
condition in which tendon reflexes are reduced and it may subside temporarily after a period of
exercise.[14]
5060% of the patients that are diagnosed with LEMS also have present an associated tumor,
which is typically small-cell lung carcinoma (SCLC). This type of tumor also expresses voltagegated calcium channels.[14] Oftentimes, LEMS also occurs alongside myasthenia gravis.[13]
Treatment for LEMS consists of using 3,4-diaminopyridine as a first measure, which serves to
increase the compound muscle action potential as well as muscle strength by lengthening the
time that voltage-gated calcium channels remain open after blocking voltage-gated potassium
channels. Further treatment includes the use of prednisone and azathioprine in the event that 3,4diaminopyridine does not aid in treatment.[14]
Neuromyotonia
Neuromyotonia (NMT), otherwise known as Isaacs syndrome, is unlike many other diseases
present at the neuromuscular junction. Rather than causing muscle weakness, NMT leads to the
hyperexcitation of motor nerves. NMT causes this hyperexcitation by producing longer
depolarizations by down-regulating voltage-gated potassium channels, which causes greater
neurotransmitter release and repetitive firing. This increase in rate of firing leads to more active
transmission and as a result, greater muscular activity in the affected individual. NMT is also
believed to be of autoimmune origin due to its associations with autoimmune symptoms in the
individual affected.[12]

Genetic
Congenital myasthenic syndromes
Congenital myasthenic syndromes (CMS) are very similar to both MG and LEMS in their
functions, but the primary difference between CMS and those diseases is that CMS is of genetic
origins. Specifically, these syndromes are diseases incurred due to mutations, typically recessive,
in 1 of at least 10 genes that affect presynaptic, synaptic, and postsynaptic proteins in the
neuromuscular junction. Such mutations usually arise in the -subunit of AChR,[12] thereby
affecting the kinetics and expression of the receptor itself. Single nucleotide substitutions or
deletions may cause loss of function in the subunit. Other mutations, such as those affecting
acetylcholinesterase and acetyltransferase, can also cause the expression of CMS, with the latter
being associated specifically with episodic apnea.[15] These syndromes can present themselves at
different times within the life of an individual. They may arise during the fetal phase, causing
fetal akinesia, or the perinatal period, during which certain conditions, such as arthrogryposis,
ptosis, hypotonia, ophthalmoplegia, and feeding or breathing difficulties, may be observed. They
could also activate during adolescence or adult years, causing the individual to develop slowchannel syndrome.[12]
Bulbospinal muscular atrophy
Bulbospinal muscular atrophy, also known as Kennedys disease, is a rare recessive
trinucleotide, polyglutamine disorder that is linked to the X chromosome. Because of its linkage
to the X chromosome, it is typically transmitted through females. However, Kennedys disease is
only present in adult males and the onset of the disease is typically later in life. This disease is
specifically caused by the expansion of a CAG-tandem repeat in exon 1 found on the androgenreceptor (AR) gene on chromosome Xq11-12. Poly-Q-expanded AR accumulates in the nuclei of
cells, where it begins to fragment. After fragmentation, degradation of the cell begins, leading to
a loss of both motor neurons and dorsal root ganglia.[16]
Symptoms of Kennedys disease include weakness and wasting of the facial bulbar and extremity
muscles, as well as sensory and endocrinological disturbances, such as gynecomastia and
reduced fertility. Other symptoms include elevated testosterone and other sexual hormone levels,
development of hyper-CK-emia, abnormal conduction through motor and sensory nerves, and
neuropathic or in rare cases myopathic alterations on biopsies of muscle cells.[16]
Duchenne muscular dystrophy
Duchenne muscular dystrophy is an X-linked genetic disorder that results in the absence of the
structural protein dystrophin at the neuromuscular junction. It affects 1 in 3,6006,000 males and
frequently causes death by the age of 30. The absence of dystrophin causes muscle degeneration,
and patients present with the following symptoms: abnormal gait, hypertrophy in the calf
muscles, and elevated creatine kinase. If left untreated, patients may suffer from respiratory
distress, which can lead to death.[17]
http://en.wikipedia.org/wiki/Neuromuscular_junction

Describe the steps involved in the contraction process. Include the

neurotransmitters, cations, and proteins.?
Firstly, when the action potential reaches the axon terminal in the neuromuscular
junction, it stimulates the synaptic vesicles to fuse with the membrane and release
ACh.
Then, ACh receptors on the sarcolemma pick up the ACh floating in the synaptic
cleft and this binding opens the chemically gated ion channels which allows NA+ to
diffuse into the cell (and some K+ diffuses out).
This diffusion of NA+ causes a change in membrane potential and depolarizes the
motor end plate.
Then, excitation-contraction coupling takes place, in these steps:
1) The action potential propagates down the sarcolemma and down the T tubules
2) Action potential in the t-tubule activates voltage-sensitive receptors which in turn
trigger CA2+ release from the terminal cisternae of the SR into the cytosol
3) Calcium ions bind to troponin, troponin changes shape, removing the blocking
action of tropomyosin and the actin active sites are exposed
4) Muscle contracts - myosin heads alternately attach to actin and detach, pulling
the actin filaments toward the center of the sarcomere; release of energy by ATP
hydrolysis powers the cycling process
5) Removal of CA2+ by active transport in to the SR after the action potential ends
6) Tropomyosin blockage is restored, blocking the myosin binding sites on actin contraction ends and muscle fiber relaxes
Source(s):
A&P class
http://answers.yahoo.com/question/index?qid=20100622233245AAA8ael
The Mechanism of Muscle Contraction
Objectives:

(1) To evaluate the nervous response needed to cause calcium to be released for muscle to
contract.
(2) To discuss the role of calcium in turning muscle on.
(3) To show the steps necessary for muscle to relax.

Reading material: Principles of Meat Science (4th Edition), chapter 4, pages 69 to 80.

Below are two different but similar descriptions of muscle contraction that explain the processes
involved in notification, contraction, and relaxation.
The following steps are involved in muscle contraction:
(1) The sequence of events leading to contraction is initiated somewhere in the central nervous
system, either as voluntary activity from the brain or as reflex activity from the spinal cord.
(2) A motor neuron in the ventral horn of the spinal cord is activated, and an action potential
passes outward in a ventral root of the spinal cord.
(3) The axon branches to supply a number of muscle fibers called a motor unit, and the action
potential is conveyed to a motor end plate on each muscle fiber.
(4) At the motor end plate, the action potential causes the release of packets or quanta of
acetylcholine into the synaptic clefts on the surface of the muscle fiber.
(5) Acetylcholine causes the electrical resting potential under the motor end plate to change, and
this then initiates an action potential which passes in both directions along the surface of the
muscle fiber.
(6) At the opening of each transverse tubule onto the muscle fiber surface, the action potential
spreads inside the muscle fiber.
(7) At each point where a transverse tubule touches part of the sarcoplasmic reticulum, it causes
the sarcoplasmic reticulum to release Ca++ ions.
(8) The calcium ions result in movement of troponin and tropomyosin on their thin filaments,
and this enables the myosin molecule heads to grab and swivel their way along the thin
filament. This is the driving force of muscle contraction.
Contraction is turned off by the following sequence of events:
(9) Acetylcholine at the neuromuscular junction is broken down by acetylcholinesterase, and this
terminates the stream of action potentials along the muscle fiber surface.
(10) The sarcoplasmic reticulum ceases to release calcium ions, and immediately starts to
resequester all the calcium ions that have been released.

(11) In the absence of calcium ions, a change in the configuration of troponin and tropomyosin
then blocks the action of the myosin molecule heads, and contraction ceases.
(12) In the living animal, an external stretching force, such as gravity or an antagonistic muscle,
pulls the muscle back to its original length.
Muscle contraction flow chart (figure 4.7)
Contraction Phase

Resting state
Motor nerve action potential arrives at motor end plate
Acetylcholine released, sarcolemma and membranes depolarized (Na+ flux into fiber)
Action potential transmitted via T-tubules to SR
Ca++ released from SR terminal cisternae into sarcoplasm
Ca++ bound by troponin
Myosin ATPase activated and ATP hydrolyzed
Tropomyosin shift from actin binding site
Actin-myosin crossbridge formation
Repeated formation & breaking of crossbridges resulting in sliding of filaments and sarcomere
shortening
Relaxation Phase
Cholinesterase released and acetylcholine breakdown

Sarcolemma & T-tubules repolarized

SR Ca++ pump activated & Ca++ returned to SR terminal cisternae
Actin-myosin crossbridge formation terminated
Return of tropomyosin to actin binding site
Mg++ complex formed with ATP
Passive sliding of filaments

Sarcomeres return to resting state

Review of Material What the student should know:

(1) The nervous events that take place in contraction.

(2) The role of calcium in turning the muscle on.
(3) The factors related to the actual contraction process.
(4) The events that take place to cause relaxation to occur.
http://meat.tamu.edu/ansc-307-honors/muscle-contraction/

Skeletal muscles are told what to do by the nervous system. They only contract when
told to do so.
You already
learned that the
electrically
active, signalling
cells of the
nervous system
are the neurons.
Neurons are cells
with many
processes sticking
off of them, and one of these processes provides the output of the electrical
information for the neuron. This output process is the thinnest process, and there is
only one of them; it is called the axon. Do you see the axon in the diagram of this
neuron to the left?
You do not need to learn all the names of the parts of the neuron yet. That will
come soon enough. All I want you to see for now is that the neuron sends its
information down its axon to its presynaptic terminals ("pre" for before, because the
information comes from this end). It's presynaptic terminals in this diagram are all at
the far right-hand edge of the drawing.
A neuron that communicates directly with a muscle is called a motor neuron
("motor" for movement). So you may also see the presynaptic terminals called the
motor neuronal terminals. With what does the motor neuron communicate? Certainly
not with the entire muscle.

Think about it this way... if one motor neuron controlled all the muscle fibers in an
entire muscle, every time that motor neuron was active, the entire muscle would
contract. Our muscular contractions would then be all-or-none. And we would move
about this world in a jerky fashion. Since that is not the case, can you figure out
what the motor neuron connects to? It connects to muscle fibers. Somewhere
between a few muscle fibers and many-- but that is the topic for the next web page
on motor units.
You should expect that if the muscle fiber receives information from a motor
neuron, it should have an anatomical specialization at the point of motor neuronal
contact. The specialized region on the muscle fiber is called the motor end plate
(that's just a fancy way of saying that it is the muscle's postsynaptic terminal, "post"
for after, because the information is received at this end).
The neuromuscular junction is the term for the connection between the nervous
system and the muscle fiber. It is a type of synapse-- a connection from a neuron to
either another neuron or a muscle or another effector organ. Regardless, it is a
connection from that sends electrical information to another place. This electrical
information has to travel from one cell to another. The problem is that each cell is an
independent unit, and there is space between the two cells that must communicate
electrically.
You probably know from experience that if you cut the electrical cord from a lamp
right in half and then plug in the half that can get plugged in, even if you put the two
halves of the cord close together, if the two halves don't touch, your light won't turn
on. (don't try this, though-- big fire hazard!) Cells that communicate electrically
have to have a gap between them in order to be different cells. So how do they
bridge this gap? They transfer the electrical information into chemical information to
cross the gap, then the chemical information is transformed back into electrical
information.
Follow along through the next description on Figure 9.7 in your textbook...
The electrical information (called an Action Potential, or AP) reaches the tip of
the motor neuronal terminal. There, the AP causes the motor neuronal terminal to
secrete a chemical. The specific chemical is called acetylcholine (or ACh). The ACh,
once secreted, simply diffuses across the gap between the motor neuron and the
muscle fiber. This gap is called the synaptic cleft, literally meaning the space within
the synapse. When the ACh reaches the motor end plate, the membrane has specific
receptors to recognize ACh, called acetylcholine receptors (or AChRs). When ACh
comes in contact with the AChRs on the motor end plate, the AChRs are able to
trigger the generation of an AP on the sarcolemma. Thus, an electrical signal is
restored postsynaptically.
To summarize what happens across the neuromuscular junction,

electrical signal
AP
on motor neuron

----->

chemical signal
ACh
in synaptic cleft

----->

electrical signal
AP
on sarcolemma

You will get a lot more detail on synapses when we cover the nervous system. Until
then, this is enough terminology.
Meanwhile, you should now be able to see that only those muscle fibers that
receive information from a particular motor neuron will be excited to contract when
that particular motor neuron is electrically active. To understand this further, go on
to the motor unit page.
http://faculty.stcc.edu/AandP/AP/AP1pages/Units5to9/Unit7/neuromus.htm
Anatomy of Neuromuscular Junctions (NMJs)
How muscles work continued ...

As explained on the previous page (The Sliding-Filament Theory of Muscle Action), muscles
contract and relax as a result of two different types of filaments (called thick filaments, and thin
filaments) moving backwards and forwards across each other.
The next question is: What causes such movements to occur ?
Muscles (and other tissues) are controlled by the nervous system - which consists of nerve cells
called neurones. Of the three types of neurones (motor neurones, sensory neurones and relay
neurones), motor neurones instruct skeletal muscle cells to perform the series of actions that lead
to sliding filaments and hence muscle contraction.
A single motor neurone together with all of the muscle fibers (muscle cells) to which it is
attached, and therefore stimulates, is called a motor unit.

Stimulation of the one neurone of a motor unit results in simultaneous contraction of all
of the muscle cells in that motor unit.

The number of muscle cells in a motor unit, i.e. the ratio of motor neurones (nerve cells)
to muscle cells, varies according to the type and function of the muscle of which it is a
part.
For example, delicate muscles of facial expression are not developed for high loadbearing actions but rather to convey a huge variety of subtle movements of skin. These
muscles therefore consist of motor units containing only a few (sometimes less than 10)
muscle cells each. However, larger more powerful muscles - such as the biceps brachii
and the gastrocnemius - contain motor units of up-to 2000 muscle cells each.

Neuromuscular junctions (NMJs) are the locations and means by which the motor neurones of
the nervous system instruct the muscle cells of the muscular system to take actions - actions that,

in turn, lead to the movement of muscles and the attached structures such tissues, bones, limbs
etc..
Anatomical Description of a NMJ:
Each neuromuscular junction consists of the axon terminal of a motor neuron and the motor end
plate of a muscle fibre.

The Motor Neurone Part:

The long processes of neurones are called "axons". As the axon of a motor neurone enters
the structure of skeletal muscle it forms many branches called "axon terminals". There is
a bulbous swelling called a "synaptic end bulb" at the extreme/end of each axon
terminal. Each synaptic end bulb contains many synaptic vesicles, each of which
contains an important chemical neurotransmitter called "acetylcholine", which is often
abbreviated to simply "ACh".

The Muscle Fiber Part:

The part of the sarcolemma of the muscle cell that is in closest proximity to the synaptic
end bulb is called the "motor end plate".

The "Synapse" or "Neuromuscular Junction" (NMJ):

The area between the axon terminal (of the neurone - nerve cell) and the sarcolemma (the plasma
membrane sheath that forms the outer-layer of the muscle cell) is called the "synaptic cleft".
In terms of the anatomy of the nervous system, the tiny gap across which nerve impulses pass
from one neuron (nerve cell) to the next is called a "synapse". A neuromuscular junction (also
known, and sometimes referred to as a "myoneural junction") is the equivalent gap between a
motor-neuron and the motor end plate of a muscle cell to which it is attached. However, in the
case of the NMJ, some texts refer to the tiny physical gap as the "synaptic cleft" and use the
term "neuromuscular junction" to refer to the interaction of the nerve and muscle cells more
generally* - and so also serve as the heading under which the processes that occur at the NMJ are
described.
* We include comment on this possibly confusing terminology because the overlapping use of
terms used here and elsewhere may be misleading.
The Oxford Medical Dictionary defines a neuromuscular junction as "the meeting point of a
nerve fibre and the muscle fibre that it supplies".