The nervous system is an elaborate network that enables us to perform functions as vital as breathing or simple as blinking. One of the most fundamental components of this body system is the neuromuscular junction.
Although the neuromuscular junction is a microscopic complex consisting of only three parts, its importance cannot be understated. As a quintessential component of life and the center of many neurological disease states, it is essential to grasp the fundamental concepts behind the physiology of the neuromuscular junction.
What Is The Neuromuscular Junction?How Does The Neuromuscular Junction Function?Disorders Of The Neuromuscular JunctionHow Do Toxins Affect The Neuromuscular Junction?Conclusion
What Is The Neuromuscular Junction?
How Does The Neuromuscular Junction Function?
Disorders Of The Neuromuscular Junction
How Do Toxins Affect The Neuromuscular Junction?
Conclusion
The neuromuscular junction, or the myoneural junction, is a three-part neuronal unit consisting of the terminal end of a motor neuron, a muscular fiber, and the motor endplate, which separates the first two parts. The role of the neuromuscular junction is to facilitate the transmission of action potentials from motor neurons to the muscle, which ultimately brings about contraction or relaxation of the muscle tissue.
To understandthe structure and physiology of the neuromuscular junction, let’s take a deeper look at each section.
The Terminal End Of The Neuromuscular Junction
The terminal end of the motor neuron consists of a large complex of branched nerve endings, which house active zones and calcium ion channels. Like all cells, motor neurons contain standard cell components such as mitochondria, endoplasmic reticulum, and synaptic vesicles.
Nerve endings, also called nerve terminals or terminal boutons, are enclosed in a cellular membrane that thickens in some areas to form active zones. These zones are a dense collection of proteins and voltage-gated calcium ion channels. Active zones are fundamental in releasing neurotransmitters from synaptic vesicles in the motor neuron into the synaptic cleft.
Like all nerve cells, motor neurons are rich in mitochondria. These cellular components are essential for various processes, including adenosine triphosphate (ATP) production, intracellular calcium ion signaling, and the formation of reactive oxygen species. These processes combine to establish the excitability of the cell membrane and facilitate plasticity and neurotransmission.
The synaptic vesicles released into the cleft in response to these intracellular changes are specialized sac-like structures that contain neurotransmitters. In motor neurons, these vesicles contain acetylcholine, one of the nervous system’s primary neurotransmitters. The expulsion of acetylcholine from a motor neuron into the synaptic cleft brings about muscular contraction.
The Synaptic Cleft Of The Neuromuscular Junction
The synaptic or junctional cleft is a space of about 50 nanometers between the muscle cell’s plasma membrane and the nerve terminal of the motor neuron. Presynaptic neurotransmitters, such as acetylcholine, are released at this location before interacting with nicotinic acetylcholine receptors on the motor endplate.
Synaptic basal lamina, a particular extracellular matrix, envelopes each muscle cell and passes between the pre-and post-synaptic membranes at the neuromuscular junction. This matrix is essential for the neuromuscular junction’s alignment, structure, and organization.
The acetylcholinesterase enzyme, which is present in the synaptic cleft of the neuromuscular junction, is in charge of breaking down the released acetylcholine so that its effect on the post-synaptic receptors is not prolonged. Ultimately, the action of this enzyme is responsible for the cessation of muscle contraction.
The Motor End Plate Of The Neuromuscular Junction
A muscle’s motor unit’s size or innervation ratio often decreases as the muscle’s necessity for fine control rises. The mass of the muscle and the rate of contraction has an impact on a motor unit’s size as well. Smaller motor units are frequently found in small muscles, while large motor units typically innervate large, strong muscles that produce significant levels of force.
However, larger muscles can also include small motor units. The small motor units are first engaged for accuracy, whereas the bigger ones are later in the action for enhanced strength.
The muscle plasma membrane’s thicker region, or sarcolemma, is folded to create depressions known as junctional folds. The nerve terminals closely fit the motor end plate to transmit neurotransmitters efficiently.
Thousands of receptors are embedded in the end plate, which are long protein molecules that form channels through the membrane. Nicotinic acetylcholine receptors are clustered at the apex of each junctional fold. These receptors are acetylcholine-gated ion channels that allow the entry of sodium ions from the fluid in the cleft into the muscular membrane.
At first glance, the neuromuscular junction’s intricacy can seem overwhelming. However, breaking down each step in transmitting neurotransmitters between the terminals shines greater clarity on this vastly complex system. Let’s look athow the neuromuscular junction brings about muscular contraction.
The enzyme choline transferase acts on choline and acetyl-CoA to produce acetylcholine in the presynaptic neuron. Acetylcholine then undergoes several changes before being packaged into the synaptic vesicles.
When the motor neuron experiences depolarization, an action potential moves down the axon. The arrival of an action potential results in the opening of voltage-gated calcium channels and a movement of calcium ions into the nerve terminal. As a result, the synaptic vesicles move toward the nerve terminal membrane and join the active zones.
The nicotinic acetylcholine receptors on the junctional folds of the motor endplate then bind to the released acetylcholine. The acetylcholine-gated ion channels open because of the binding, allowing sodium ions to enter the muscle. The sodium inflow alters the post-synaptic membrane potential from -90 mV to -45 mV.
Endplate potential refers to this drop in membrane potential. Endplate potential in the neuromuscular junction is powerful enough to cause an action potential to spread across the skeletal muscle membrane, which eventually causes muscle contraction.
“Neuromuscular diseases” refers to any condition affecting synaptic communication between a motor neuron and a muscle cell. These illnesses range in severity and fatality and can be inherited or acquired.
Myasthenia gravis, an autoimmune disease, causes the body to produce antibodies against either the acetylcholine receptor or against a specialized enzyme present in the motor end plate, known as a post-synaptic muscle-specific kinase.
These changes in neurotransmission cause greater neurotransmitter release and repetitive firing. This increase in the firing rate leads to more active transmission and, as a result, greater muscular activity in the affected individual.
Congenital myasthenic syndromes are very similar to myasthenia gravis and Lambert-Eaton myasthenic syndrome in their functions, but the primary difference between the diseases is that genetic mutations cause congenital myasthenic syndromes. These syndromes can present themselves at different times within an individual’s life.
Botox is one of the best-known examples of such advancements. By interfering with synaptotagmin and synaptobrevin,botulinum toxinprevents the release of acetylcholine at the neuromuscular junction. As a result, the muscle experiences localized chemical denervation and a brief flaccid paralysis.
The suppression of acetylcholine release begins around two weeks following the injection. The neuronal activity starts to restore function three months after the inhibition partially, and total neuronal function is returned after six months.
Both the release of calcium ions and the formation of pores raise the calcium level in the presynaptic cell, which subsequently triggers the release of acetylcholine-containing synaptic vesicles. If left untreated, latrotoxin can result in paralysis and death, as well as extreme pain, muscular tightness, and death.
At the neuromuscular junction,snake venomacts as a toxin that can cause weakness and paralysis. Presynaptic neurotoxins prevent neurotransmitters like acetylcholine from entering the synaptic cleft between neurons. Some of these toxins, nevertheless, are also known to promote the release of neurotransmitters.
This effectively prevents the opening of sodium channels connected to these acetylcholine receptors, causing a neuromuscular blockade comparable to the effects of presynaptic neurotoxins. The muscles engaged in the impacted connections become paralyzed as a result.
Post-synaptic neurotoxins are more susceptible to anti-venoms than presynaptic neurotoxins, which speed up the toxin’s separation from the receptors and eventually reverse paralysis. These neurotoxins help in research on acetylcholine as well as studies of myasthenia gravis patients.
References
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5816724/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3743085/
https://www.sciencedirect.com/science/article/abs/pii/S1044578106800265
https://www.sciencedirect.com/topics/medicine-and-dentistry/motor-end-plate
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Reference this article:Practical Psychology. (2022, August).Neuromuscular Junction.Retrieved from https://practicalpie.com/neuromuscular-junction/.Practical Psychology. (2022, August). Neuromuscular Junction. Retrieved from https://practicalpie.com/neuromuscular-junction/.Copy
Reference this article:
Practical Psychology. (2022, August).Neuromuscular Junction.Retrieved from https://practicalpie.com/neuromuscular-junction/.Practical Psychology. (2022, August). Neuromuscular Junction. Retrieved from https://practicalpie.com/neuromuscular-junction/.Copy
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