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→神经肌肉接头Neuromuscular junctions
有些突触免除了神经递质的“中间人”，而将突触前细胞和突触后细胞连接在一起。<ref name=":9" group="lower-alpha" /> 当一个动作电位达到这样的突触时，流入突触前细胞的离子电流可以穿过两个细胞膜的屏障，通过称为连接子的孔进入突触后细胞。<ref name=":10" group="lower-alpha" /> 因此，突触前动作电位的离子电流可以直接刺激突触后细胞。电突触允许更快的传递，因为它们不需要神经递质在突触间隙中的缓慢扩散。因此，只要快速反应和协调时间是至关重要的，就会使用电突触，例如在逃跑反射、脊椎动物的视网膜和心脏中。
有些突触免除了神经递质的“中间人”，而将突触前细胞和突触后细胞连接在一起。<ref name=":9" group="lower-alpha" /> 当一个动作电位达到这样的突触时，流入突触前细胞的离子电流可以穿过两个细胞膜的屏障，通过称为连接子的孔进入突触后细胞。<ref name=":10" group="lower-alpha" /> 因此，突触前动作电位的离子电流可以直接刺激突触后细胞。电突触允许更快的传递，因为它们不需要神经递质在突触间隙中的缓慢扩散。因此，只要快速反应和协调时间是至关重要的，就会使用电突触，例如在逃跑反射、脊椎动物的视网膜和心脏中。
===神经肌肉接头Neuromuscular junctions===
===神经肌肉接头===
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" name=":11">{{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" name=":12">{{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" name=":13">{{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>
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" name=":11">{{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" name=":12">{{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" name=":13">{{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>
突触间隙的一个特例是神经肌肉接点（neuromuscular junction），运动神经元的轴突终止于肌纤维上。<ref name=":11" group="lower-alpha" /> 在这种情况下，释放出来的神经递质是乙酰胆碱，它结合在肌肉纤维膜（肌膜）上的内在膜蛋白乙酰胆碱受体。<ref name=":12" group="lower-alpha" /> 然而，乙酰胆碱并不保持结合状态，而是解离并被位于突触中的乙酰胆碱酯酶水解。这种酶能迅速减少对肌肉的刺激，从而使肌肉收缩的程度和时间得到精细的调节。一些毒药使乙酰胆碱酯酶失活，以阻断这种控制，如神经毒剂沙林和塔崩，<ref name="Newmark" group="lower-alpha" /> 以及杀虫剂二嗪农和马拉硫磷。<ref name=":13" group="lower-alpha" />
突触间隙的一个特例是神经肌肉接点（neuromuscular junction），运动神经元的轴突终止于肌纤维上。<ref name=":11" group="lower-alpha" /> 在这种情况下，释放出来的神经递质是乙酰胆碱，它结合在肌肉纤维膜（肌膜）上的内在膜蛋白乙酰胆碱受体。<ref name=":12" group="lower-alpha" /> 然而，乙酰胆碱并不保持结合状态，而是解离并被位于突触中的乙酰胆碱酯酶水解。这种酶能迅速减少对肌肉的刺激，从而使肌肉收缩的程度和时间得到精细的调节。一些毒药使乙酰胆碱酯酶失活，以阻断这种控制，如神经毒剂沙林（[[sarin]]）和塔崩（tabun），<ref name="Newmark" group="lower-alpha" /> 以及杀虫剂二嗪农（[[diazinon]]）和马拉硫磷（[[malathion]]）。<ref name=":13" group="lower-alpha" />
==Other cell types 其他细胞类型==
==其他细胞类型==
===Cardiac action potentials 心肌动作电位===
===心肌动作电位===
[[Image:Ventricular myocyte action potential.svg|thumb|220px|[[文件:Ventricular myocyte action potential.svg.png|缩略图]]Phases of a cardiac action potential. The sharp rise in voltage （"0"） corresponds to the influx of sodium ions, whereas the two decays （"1" and "3", respectively） correspond to the sodium-channel inactivation and the repolarizing eflux of potassium ions. The characteristic plateau （"2"） results from the opening of voltage-sensitive [[calcium]] channels.
[[Image:Ventricular myocyte action potential.svg|thumb|220px|[[文件:Ventricular myocyte action potential.svg.png|缩略图]]Phases of a cardiac action potential. The sharp rise in voltage （"0"） corresponds to the influx of sodium ions, whereas the two decays （"1" and "3", respectively） correspond to the sodium-channel inactivation and the repolarizing eflux of potassium ions. The characteristic plateau （"2"） results from the opening of voltage-sensitive [[calcium]] channels.