The neuromuscular junction (NMJ) is a synapse-specific, dynamic cellular communication pathway between a muscle contraction motor nerve and the corresponding muscle. The neuromuscular junction is a broad communication channel between different sets of bones, muscles, and tendons. It controls the action of impulses transmitted through the axon to the projection areas of the muscle fibers. In this brief article, the NMJ of skeletal muscles will be briefly discussed.
Skeletal muscle weakness results from damage or inflammation of the neuromuscular junction. Neuromuscular Junction is composed of myofibrils, which are protein-filled vesicles on the axon's ends, along with tensor fascia, which is fibrous tissue around the insertion sites muscles. The destruction of these structures results in the loss of myofibrils and eventually weakens the muscles.
The formation of the neuromuscular junction requires three critical steps. First, a synapse is formed between two pre-existing synapses. The synapse is established by the growth of a receptor on one of the presynaptic terminals. Secondly, a chemical messenger is transported from the presynapse to the axon terminal. Finally, the glial cells - specialized cells that give rise to new myogenic cells - arrive at the junction to mediate neurotransmitters' synthesis and release.
The growth of the receptor and the subsequent formation of a synapse depend upon the strength of the force applied to the nerve. Neuromuscular Junction is formed when the force applied to the nerve breaks a water molecule called the "intrinsic pyrophosphate." When this happens, the level of available ATP is reduced, and the process of biogenesis ensues. When the ATP concentration has been restored, the strength of the force can be restored, and the process continues.
Neuromuscular Junction creates a synapse when two different types of muscle contraction are combined. This is true for all types of muscular contraction, including muscular contractions not caused by external stimuli. This type of synchronicity allows for the synapses to increase in size, synapsis, and the number of fibers present in the developing neuromuscular junction. More neurons are added to the overall number of neurons in the developing brain and spinal cord as more muscles contract.
Neuromuscular Junction has been linked to several diseases such as autism, diabetes, arthritis, stroke, heart disease, obesity, asthma, epilepsy, Lou Gehrig's Disease, Huntington's Disease, Parkinson's disease, multiple sclerosis, rheumatoid arthritis, and fibromyalgia. Neuromuscular Arthritis is the most common form of this disease. The disease occurs when the protective cartilage at the ends of the neuromuscular junction is destroyed, leaving behind a scar. When this happens, the endplate potential of the musculoskeletal system is decreased, and the risk for the disease increases significantly.
Neuromuscular Arthritis occurs when the myelin sheath around the neuromuscular junction is damaged. The inflammation leads to decreased conductivity and strength, as well as to a decreased ability for motor neurons to send signals. Once the myelin sheath surrounding the neuromuscular junction is damaged, messages cannot be sent from the brain correctly. These messages cause the motor neurons to stop sending the proper signals to the rest of the body. If this happens, the muscles will no longer be able to perform the movements that they should be performing and can even become paralyzed.
Neuromuscular Arthritis occurs when damage occurs at the level of the neuromuscular junction. It can occur inside the axon or between the axon and the presynaptic terminal. The condition often begins to show symptoms during childhood and continues into adulthood. The most common form of Neuromuscular Arthritis is called idiopathic myopathy, which is caused by a decreased number of neurotransmitters in the central nervous system. In contrast, primary progressive myopathy, which develops over time, is idiopathic in nature.