The neuromuscular junction: Structure and function
The activation of many muscle fibers together causes muscles to contract, which in turn can produce movement. The neuromuscular junction then, is a key component in the body’s ability to produce and control movement. Amazingly, processes at the neuromuscular junction take place at speeds that allow movements to occur with no appreciable delay or lag.
This article will discuss the anatomy and function of the neuromuscular junction.
- Synaptic end bulb
- Motor end plate
- Synaptic cleft
- Clinical significance
Each muscle is surrounded by a thin sheet of connective tissue or fascia known as epimysium. Within the muscle, bundles of muscle fibers or cells, known as fascicles, are bound together by another layer of connective tissue known as the perimysium. Every muscle fiber or cell within a fascicle is itself encased in a layer of connective tissue called endomysium
Each individual muscle fiber is innervated (supplied) and controlled by a motor neuron. This motor neuron, which has its cell body located within the central nervous system, will have axons that enter the muscle and penetrate the perimysium.
At this point, each axon of the motor neuron will divide into branches called axon terminals. Towards the end of the axon terminal, closest to the muscle fiber, the tip of the axon terminal enlarges and becomes known as the synaptic end bulb. It is the synaptic end bulb of the motor neuron that comprises the nervous system component of the neuromuscular junction. The muscular component is a region of the muscle fiber referred to as the motor end plate. Between the synaptic end bulbs of the neuron and the cell membrane of the muscle fiber (the sarcolemma) lies a space known as the synaptic cleft, which is the final component of the neuromuscular junction.
Synaptic end bulb
The presence of the synaptic cleft between the synaptic end bulb of the neuron and the motor end plate of the muscle fiber, means that the electrical signal or action potential, arriving from the central nervous system, needs to somehow transverse (cross) this space. The neuromuscular junction accomplishes this by turning the electrical signal from the nervous system into a chemical signal that can be moved across the synaptic cleft.
The chemical in this case is acetylcholine (ACh), an example of a neurotransmitter that allows neurons to communicate with other cells. ACh is stored inside the synaptic end bulb within membrane-enclosed sacs known as synaptic vesicles. As the electrical signal approaches the synaptic end bulb, it stimulates the inflow of calcium (Ca2+) by opening voltage-gated channels in the cell membrane of the neuron.
The increase of Ca2+ within the cytosol of the synaptic end bulb causes the synaptic vesicles to move towards and fuse with the neuron’s cell membrane. Once fused, the synaptic vesicles exocytose (release) their contents – ACh – into the synaptic cleft. The ACh then moves across the synaptic cleft towards the motor end plate of the muscle fiber.
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Motor end plate
Across the synaptic cleft from the synaptic end bulb is a specialized region of the muscle fiber sarcolemma known as the motor end plate (postsynaptic membrane). There is one neuromuscular junction associated with each muscle fiber, and it is typically located near the middle of the fiber. This means that the motor end plate will also be located near the midpoint of the muscle fiber.
The motor end plate has two specializations that make it ideal for receiving ACh released from the synaptic end bulb.
- The first specialization at the motor end plate is the presence of junctional folds, which are deep invaginations or grooves of the sarcolemma that provide a large surface area where the ACh from the synaptic end bulb can interact.
- Secondly, within the region of the motor end plate, the sarcolemma of the junctional folds contains 30 to 40 million acetylcholine receptors. These receptors are integral transmembrane proteins that function as an ion channel once activated.
The binding of two molecules of ACh to an acetylcholine receptor, opens the ion channel in the receptor and allows the influx of sodium (Na+) into the muscle fiber. It is this influx of Na+ that once again initiates an electrical impulse or action potential that travels outwards from the motor end plate towards both ends of the muscle fiber causing the muscle fiber to contract and shorten.
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Up until now the synaptic cleft has merely been a space between the neural and muscular components of the neuromuscular junction. It does however, house an enzyme that is imperative for the proper function of muscles.
If ACh remained within the synaptic cleft, it would continue to bind to acetylcholine receptors in the motor end plate region causing continued muscle contraction. Instead, the synaptic cleft contains acetylcholinesterase (AChE), an enzyme that breaks down ACh into acetyl and choline, neither of which can activate the acetylcholine receptors.
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A number of the events that occur at the neuromuscular junction can be affected by either plant products or drugs. For example, the botulinum toxin, which is produced by the bacteria Clostridium botulinum, blocks the release of ACh from the synaptic vesicles contained within the synaptic end bulb. With no ACh present in the synaptic cleft and no binding to acetylcholine receptors within the motor end plate region, muscle contraction does not occur, essentially paralyzing the victim, stopping respiration and leading to death.
This bacterium can occur due to improperly canned foods and the toxin it produces is one of the most lethal known. It can also be selectively used in medicine however (Botox®), to relax muscles that may be causing strabismus (crossed eyes), blepharospasm (uncontrollable blinking), or problems with speech due to vocal cord spasm.
Curare, a plant based poison, can also cause muscle paralysis by binding to and blocking ACh receptors within the motor end plate of the muscle fiber. In this case, ACh is present, but it cannot activate and open the ion channels that allow the influx of Na+ which initiates the action potential in the muscle fiber. Drugs with curare-like properties can also be used therapeutically during surgery to relax musculature.
Rather than causing paralysis, other chemicals can be used to strengthen weak muscle contractions if necessary, such as in myasthenia gravis. These anticholinesterase agents act by slowing the activity of AChE, which in turn slows the removal of ACh from the synaptic cleft. With ACh lingering in the synaptic cleft, it will continue to bind to ACh receptors and strengthen muscle contraction.
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