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{{short description|Voltages associated with muscle fibre}}[[File:Sample_EPP_and_mEPPs.jpg|thumb|A sample endplate potential (EPP; an average of 10 single EPPs) is shown at the top, and sample miniature endplate potentials (mEPPs) are shown at the bottom. Note the differences in the scales on the X- and Y-axes. Both are taken from recordings at the mouse neuromuscular junction.]]
'''End plate potentials''' ('''EPPs''') are the voltages which cause depolarization of [[skeletal muscle]] fibers caused by [[neurotransmitters]] binding to the postsynaptic membrane in the [[neuromuscular junction]]. They are called "end plates" because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. When an [[action potential]] reaches the [[axon terminal]] of a [[motor neuron]], vesicles carrying neurotransmitters (mostly [[acetylcholine]]) are [[Exocytosis|exocytosed]] and the contents are released into the neuromuscular junction. These neurotransmitters bind to receptors on the postsynaptic membrane and lead to its depolarization. In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small depolarizations in the postsynaptic membrane. This small response (~0.4mV)<ref>{{Cite book|title=Medical Physiology|last1=Boron|first1=W.|last2=Boulpaep|first2=E.|publisher=Saunders, Elsevier inc.|year=2012|isbn=978-0-8089-2449-4|location=Philadelphia, PA|pages=224}}</ref> is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. It represents the smallest possible depolarization which can be induced in a muscle.
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===Acetylcholine===
End plate potentials are produced almost entirely by the neurotransmitter acetylcholine in skeletal muscle. Acetylcholine is the second most important excitatory neurotransmitter in the body following [[glutamate]]. It controls the [[somatosensory system]] which includes the senses of touch, vision, and hearing. It was the first neurotransmitter to be identified in 1914 by [[Henry Hallett Dale|Henry Dale]]. Acetylcholine is synthesized in the cytoplasm of the neuron from [[choline]] and [[acetyl-CoA]]. [[Choline
|title= Enhanced acetylcholine secretion in neuroblastoma X glioma hybrid NG108-15 cells transfected with rat choline-acetyltransferase CDNA
|journal=FEBS Letters
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Threshold is when the summation of MEPPs reaches a certain potential and induces the opening of the voltage-gated ion channels. The rapid influx of sodium ions causes the membrane potential to reach a positive charge. The potassium ion channels are slower-acting than the sodium ion channels and so as the membrane potential starts to peak, the potassium ion channels open and causes an outflux of potassium to counteract the influx of sodium. At the peak, the outflux of potassium equals the influx of sodium, and the membrane does not change polarity.
During repolarization, the sodium channels begin to become inactivated, causing a net efflux of potassium ions. This causes the membrane potential to drop down to its resting membrane potential of -100mV. Hyperpolarization occurs because the slow-acting potassium channels take longer to deactivate, so the membrane overshoots the [[resting potential]]. It gradually returns to resting potential and is ready for another action potential to occur.
During the action potential before the hyperpolarization phase, the membrane is unresponsive to any stimulation. This inability to induce another action potential is known as the absolute refractory period. During the hyperpolarization period, the membrane is again responsive to stimulations but it requires a much higher input to induce an action potential. This phase is known as the relative refractory period.
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|pages=543–556|pmid= 15036049|s2cid=43828995 }}</ref>
[[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 EPPs due to less vesicles being released. Often the smaller EPPs do not reach threshold which causes muscle weakness and fatigue in patients.
Many animals use
[[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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