The neuromuscular junctions are in all humans and control skeletal muscles and smooth muscles. Skeletal muscles are attached and anchored to the bones, so when they are signaled to constrict, they work similar to a levy system and cause the human body to move (Martyn et. al, 1993). The smooth muscles, however, are not involved with bodily movement; smooth muscles are involved with involuntary function. Both muscle groups are equally important and both require the neuromuscular junction in order to begin performing. With improper functioning of all the previously mentioned mechanisms, the chemical signaling to muscles would cause the muscle to perform inefficiently or not be able to perform at all. This can cause paralysis in the skeletal muscles,
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al, 2004). A metabolic impairment of the neuromuscular junction can be caused by the lack of AChE or mutation in AChE that makes the enzyme not able to hydrolyze acetylcholine, so now it remains present in the cell. This is problematic because stimulation of a receptor results in the receptor becoming less efficient at producing a signal. The immune mediated cause for neuromuscular junction malfunction is due to the body attacking the acetylcholine receptors. In the acquired immunity process, an immune cell undergoes specialization so that it can produce antibodies that correlate to foreign threats that can enter the body. Sometimes, this process malfunctions, and this creates an autoimmune disease. In this case, antibodies are produced that attack the acetylcholine receptors, and this leads to a decrease of acetylcholine receptors (Fambrough et. al, 1973). Since the neurons are not effectively recognizing the acetylcholine, it causes the person suffering with this condition to have impaired movement, or weakness. The name of that condition is called myasthenia gravis. Myasthenia gravis can become especially troublesome if the muscles that control breathing are weakened to a severe extent. Treatment for this condition involves immunosuppressant drugs to reduce the amount
al, 2004). A metabolic impairment of the neuromuscular junction can be caused by the lack of AChE or mutation in AChE that makes the enzyme not able to hydrolyze acetylcholine, so now it remains present in the cell. This is problematic because stimulation of a receptor results in the receptor becoming less efficient at producing a signal. The immune mediated cause for neuromuscular junction malfunction is due to the body attacking the acetylcholine receptors. In the acquired immunity process, an immune cell undergoes specialization so that it can produce antibodies that correlate to foreign threats that can enter the body. Sometimes, this process malfunctions, and this creates an autoimmune disease. In this case, antibodies are produced that attack the acetylcholine receptors, and this leads to a decrease of acetylcholine receptors (Fambrough et. al, 1973). Since the neurons are not effectively recognizing the acetylcholine, it causes the person suffering with this condition to have impaired movement, or weakness. The name of that condition is called myasthenia gravis. Myasthenia gravis can become especially troublesome if the muscles that control breathing are weakened to a severe extent. Treatment for this condition involves immunosuppressant drugs to reduce the amount