Editing Action potential (section)

==Termination==

===Chemical synapses===
{{Main|Chemical synapse|Neurotransmitter|Excitatory postsynaptic potential|Inhibitory postsynaptic potential}}

In general, action potentials that reach the synaptic knobs cause a [[neurotransmitter]] to be released into the synaptic cleft.<ref group=lower-alpha>{{cite book | vauthors = Süudhof TC | chapter = Neurotransmitter Release | title = Pharmacology of Neurotransmitter Release | volume = 184 | issue = 184 | pages = 1–21 | year = 2008 | pmid = 18064409 | doi = 10.1007/978-3-540-74805-2_1 | isbn = 978-3-540-74804-5 | series = Handbook of Experimental Pharmacology }}</ref> Neurotransmitters are small molecules that may open ion channels in the postsynaptic cell; most axons have the same neurotransmitter at all of their termini. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane; the influx of calcium causes [[synaptic vesicle|vesicles]] filled with neurotransmitter to migrate to the cell's surface and [[exocytosis|release their contents]] into the [[synaptic cleft]].<ref group=lower-alpha>{{cite journal | vauthors = Rusakov DA | title = Ca2+-dependent mechanisms of presynaptic control at central synapses | journal = The Neuroscientist | volume = 12 | issue = 4 | pages = 317–26 | date = August 2006 | pmid = 16840708 | pmc = 2684670 | doi = 10.1177/1073858405284672 }}</ref> This complex process is inhibited by the [[neurotoxin]]s [[tetanospasmin]] and [[botulinum toxin]], which are responsible for [[tetanus]] and [[botulism]], respectively.<ref group=lower-alpha>{{cite journal | vauthors = Humeau Y, Doussau F, Grant NJ, Poulain B | title = How botulinum and tetanus neurotoxins block neurotransmitter release | journal = Biochimie | volume = 82 | issue = 5 | pages = 427–46 | date = May 2000 | pmid = 10865130 | doi = 10.1016/S0300-9084(00)00216-9 }}</ref>

[[Image:Gap cell junction-en.svg|thumb|right|[[Electrical synapse]]s between excitable cells allow ions to pass directly from one cell to another, and are much faster than [[chemical synapse]]s.|alt=Electrical synapases are composed of protein complexes that are imbedded in both membranes of adjacent neurons and thereby provide a direct channel for ions to flow from the cytoplasm of one cell into an adjacent cell.]]

===Electrical synapses===
{{Main|Electrical synapse|Gap junction|Connexin}}

Some synapses dispense with the "middleman" of the neurotransmitter, and connect the presynaptic and postsynaptic cells together.<ref group=lower-alpha>{{cite journal | vauthors = Zoidl G, Dermietzel R | title = On the search for the electrical synapse: a glimpse at the future | journal = Cell and Tissue Research | volume = 310 | issue = 2 | pages = 137–42 | date = November 2002 | pmid = 12397368 | doi = 10.1007/s00441-002-0632-x | s2cid = 22414506 }}</ref> When an action potential reaches such a synapse, the ionic currents flowing into the presynaptic cell can cross the barrier of the two cell membranes and enter the postsynaptic cell through pores known as [[connexon]]s.<ref group=lower-alpha>{{cite journal | vauthors = Brink PR, Cronin K, Ramanan SV | title = Gap junctions in excitable cells | journal = Journal of Bioenergetics and Biomembranes | volume = 28 | issue = 4 | pages = 351–8 | date = August 1996 | pmid = 8844332 | doi = 10.1007/BF02110111 | s2cid = 46371790 }}</ref> Thus, the ionic currents of the presynaptic action potential can directly stimulate the postsynaptic cell. Electrical synapses allow for faster transmission because they do not require the slow diffusion of [[neurotransmitter]]s across the synaptic cleft. Hence, electrical synapses are used whenever fast response and coordination of timing are crucial, as in [[escape reflex]]es, the [[retina]] of [[vertebrate]]s, and the [[heart]].

===Neuromuscular junctions===
{{Main|Neuromuscular junction|Acetylcholine receptor|Cholinesterase enzyme}}

A special case of a chemical synapse is the [[neuromuscular junction]], in which the [[axon]] of a [[motor neuron]] terminates on a [[muscle fiber]].<ref group=lower-alpha>{{cite journal | vauthors = Hirsch NP | title = Neuromuscular junction in health and disease | journal = British Journal of Anaesthesia | volume = 99 | issue = 1 | pages = 132–8 | date = July 2007 | pmid = 17573397 | doi = 10.1093/bja/aem144 | df = dmy-all | doi-access = free }}</ref> In such cases, the released neurotransmitter is [[acetylcholine]], which binds to the acetylcholine receptor, an integral membrane protein in the membrane (the ''[[sarcolemma]]'') of the muscle fiber.<ref group=lower-alpha>{{cite journal | vauthors = Hughes BW, Kusner LL, Kaminski HJ | title = Molecular architecture of the neuromuscular junction | journal = Muscle & Nerve | volume = 33 | issue = 4 | pages = 445–61 | date = April 2006 | pmid = 16228970 | doi = 10.1002/mus.20440 | s2cid = 1888352 }}</ref> However, the acetylcholine does not remain bound; rather, it dissociates and is [[hydrolysis|hydrolyzed]] by the enzyme, [[acetylcholinesterase]], located in the synapse. This enzyme quickly reduces the stimulus to the muscle, which allows the degree and timing of muscular contraction to be regulated delicately. Some poisons inactivate acetylcholinesterase to prevent this control, such as the [[nerve agent]]s [[sarin]] and [[tabun (nerve agent)|tabun]],<ref name=Newmark group=lower-alpha>{{cite journal | vauthors = Newmark J | title = Nerve agents | journal = The Neurologist | volume = 13 | issue = 1 | pages = 20–32 | date = January 2007 | pmid = 17215724 | doi = 10.1097/01.nrl.0000252923.04894.53 | s2cid = 211234081 }}</ref> and the insecticides [[diazinon]] and [[malathion]].<ref group=lower-alpha>{{cite journal | vauthors = Costa LG | title = Current issues in organophosphate toxicology | journal = Clinica Chimica Acta; International Journal of Clinical Chemistry | volume = 366 | issue = 1–2 | pages = 1–13 | date = April 2006 | pmid = 16337171 | doi = 10.1016/j.cca.2005.10.008 }}</ref>