Clinical Applications
Current research is attempting to learn more about end plate potentials and their effect on muscle activity. Many current diseases involve disrupted end plate potential activity. In Alzheimer patients, beta amyloid attaches to the acetylcholine receptors and inhibits acetylcholine binding. This causes less signal propagation and small EPPs that do not reach threshold. By analyzing brain processes with acetylcholine, doctors can measure how much beta amyloid is around and use it to judge its effects on Alzheimer’s. Myasthenia gravis is an autoimmune disease, where the body produces antibodies targeted against the acetylcholine receptor on the postsynaptic membrane in the neuromuscular junction. Muscle fatigue and weakness, worsened with use and improved by rest, is the hallmark of the disease. Because of the limited amount of acetylcholine receptors that are available for binding, symptomatic treatment consists of using a acetylcholinesterase inhibitor to reduce the breakdown of acetycholine in the neuromuscular junction, so that enough acetylcholine will be present for the small number of unblocked receptors A congenital abnormality caused by a deficiency in end-plate acetylcholine esterase (AChE) might be a pathophysiologic mechanism for myasthenic gravis. In a study on a patient with AChE deficiency, doctors noted that he had developed severe proximal and truncal muscle weakness with jittering in other muscles. It was found that a combination of the jitter and blocking rate of the acetylcholine receptors caused a reduced end-plate potential similar to what is seen in cases of myasthenia gravis. Research of motor unit potentials (MUPs) has led to possible clinical applications in the evaluation of the progression of pathological diseases to myogenic or neurogenic origins by measuring the irregularity constant related. Motor unit potentials are the electrical signals produced by motor units that can be characterized by amplitude, duration, phase, and peak, and the irregularity coefficient (IR) is calculated based on the peak numbers and amplitudes. Lambert-Eaton myasthenic syndrome is a disorder where presynaptic calcium channels are subjected to autoimmune destruction which causes fewer neurotransmitter vesicles to be exocytosed. This causes smaller EEPs due to less vesicles being released. Oftentimes the smaller EPPs do not reach threshold which causes muscle weakness and fatigue in patients. Many animals use neurotoxins to defend themselves and kill prey. Tetrodotoxin is a poison found in the certain poisonous fishes such as pufferfish and triggerfish which blocks the sodium ion channels and prevents an action potential on the postsynaptic membrane. Tetraethylammonium found in insects blocks potassium channels. Alpha neurotoxin found in snakes binds to acetylcholine receptors and prevents acetylcholine from binding. Alpha-latrotoxin found in black widow spiders causes a massive influx of calcium at the axon terminal and leads to an overflow of neurotransmitter release. Botulinum toxin produced by the bacteria Clostridium botulinum is the most powerful toxic protein. It prevents release of acetylcholine at the neuromuscular junction by inhibiting docking of the neurotransmitter vesicles.
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