Neuromuscular junction disease

Neuromuscular junction disease is a medical condition where the normal conduction through the neuromuscular junction fails to function correctly. Neuromuscular junction disease is a medical condition where the normal conduction through the neuromuscular junction fails to function correctly. In diseases such as myasthenia gravis, the end plate potential (EPP) fails to effectively activate the muscle fiber due to an autoimmune reaction against acetylcholine receptors, resulting in muscle weakness and fatigue. Myasthenia gravis is caused most commonly by auto-antibodies against the acetylcholine receptor. It has recently been realized that a second category of gravis is due to auto-antibodies against MuSK. A different condition, Lambert-Eaton myasthenic syndrome, is usually associated with presynaptic antibodies to the voltage-dependent calcium channel. It is possible for these conditions to coexist. The neuromuscular junction is a specialized synapse between a neuron and the muscle it innervates. It allows efferent signals from the nervous system to contact muscle fibers causing them to contract. In vertebrates, the neuromuscular junction is always excitatory, therefore to stop contraction of the muscle, inhibition must occur at the level of the efferent motor neuron. In other words, the inhibition must occur at the level of the spinal cord. Release of acetylcholine vesicles from the presynaptic terminal occurs only after adequate depolarization of the efferent nerve. Once a motor nerve action potential reaches the presynaptic nerve terminal it causes an increase in intracellular calcium concentration by causing an increase in ion conductance through voltage gated calcium channels. This increase in calcium concentration allows the acetylcholine vesicles to fuse with the plasma membrane at the presynaptic membrane, in a process called exocytosis, thus releasing acetylcholine into the synapse. Once acetylcholine is present in the synapse it is able to bind to nicotinic acetylcholine receptors increasing conductance of certain cations, sodium and potassium in the postsynaptic membrane and producing an excitatory end т и ироооurrent. As cations flow into the postsynaptic cell, this causes a depolarization, as the membrane voltage increases above normal resting potential. If the signal is of sufficient magnitude, than an action potential will be generated post synaptically. The action potential will propagate through the sarcolemma to the interior of the muscle fibers eventually leading to an increase in intracellular calcium levels and subsequently initiating the process of Excitation–contraction coupling. Once coupling begins it allows the sarcomeres of the muscles to shorten, thus leading to the contraction of the muscle.