查看Ch14 The Autonomic Nervous System的源代码

=== 节后交感神经和副交感神经神经元通常具有毒蕈碱受体和烟碱受体 ===
<b style=color:#0ae>Postganglionic sympathetic and parasympathetic neurons often have muscarinic as well as nicotinic receptors</b>

The simplified scheme described in the preceding discussion is very useful for understanding the function of the ANS. However, two additional layers of complexity are superimposed on this scheme. First, some postganglionic neurons, both sympathetic and parasympathetic, have muscarinic in addition to nicotinic receptors. Second, at all levels of the ANS, certain neurotransmitters and postsynaptic receptors are neither cholinergic nor adrenergic. We discuss the first exception in this section and the second in the following section.

前面讨论中描述的简化方案对于理解 ANS 的功能非常有用。但是，此方案上还叠加了另外两层复杂性。首先，一些节后神经元，包括交感神经和副交感神经，除了烟碱受体外，还含有毒蕈碱。其次，在 ANS 的所有水平上，某些神经递质和突触后受体既不是胆碱能的，也不是肾上腺素能的。我们将在本节中讨论第一个异常，在下一节中讨论第二个异常。


If we stimulate the release of ACh from preganglionic neurons or apply ACh to an autonomic ganglion, many postganglionic neurons exhibit both nicotinic and muscarinic responses. Because nicotinic receptors (N2) are ligand-gated ion channels, nicotinic neurotransmission causes a fast, monophasic excitatory postsynaptic potential (EPSP). In contrast, because muscarinic receptors are GPCRs, neurotransmission by this route leads to a slower electrical response that can be either inhibitory or excitatory. Thus, depending on the ganglion, the result is a multiphasic postsynaptic response that can be a combination of a fast EPSP through a nicotinic receptor plus either a slow EPSP or a slow inhibitory postsynaptic potential (IPSP) through a muscarinic receptor. Figure 14-9A shows a fast EPSP followed by a slow EPSP.

如果我们刺激节前神经元释放 ACh 或将 ACh 应用于自主神经节，许多节后神经元会同时表现出烟碱和毒蕈碱反应。因为烟碱受体 （N2） 是配体门控离子通道，所以烟碱神经传递会导致快速、单相兴奋性突触后电位 （EPSP）。相反，由于毒蕈碱受体是 GPCR，因此通过这种途径进行的神经传递会导致较慢的电反应，这可能是抑制性的或兴奋性的。因此，根据神经节的不同，结果是多相突触后反应，可以是通过烟碱受体的快速 EPSP 加上通过毒蕈碱受体的慢速 EPSP 或慢速抑制性突触后电位 （IPSP） 的组合。图 14-9A 显示了一个快速 EPSP 后跟一个慢速 EPSP。


A well-characterized effect of muscarinic neurotransmission in autonomic ganglia is inhibition of a specific K+ current called the M current. The M current is widely distributed in visceral end organs, autonomic ganglia, and the CNS. In the baseline state, the K+ channel that underlies the M current is active and thereby produces slight hyperpolarization. In the example shown in Figure 14-9B, with the stabilizing M current present, electrical stimulation of the neuron causes only a single spike. If we now add muscarine to the neuron, activation of the muscarinic receptor turns off the hyperpolarizing M current and thus leads to a small depolarization. If we repeat the electrical stimulation in the continued presence of muscarine (see Fig. 14-9C), repetitive spikes appear because loss of the stabilizing influence of the M current increases the excitability of the neuron. The slow, modulatory effects of muscarinic responses greatly enhance the ability of the ANS to control visceral activity beyond what could be accomplished with only fast nicotinic EPSPs.

毒蕈碱神经传递在自主神经节中的一个明确特征的作用是抑制称为 M 电流的特定 K+ 电流。M 电流广泛分布于内脏终末器官、自主神经节和 CNS。在基线状态下，作为 M 电流基础的 K+ 通道是有效的，因此会产生轻微的超极化。在图 14-9B 所示的示例中，在存在稳定 M 电流的情况下，神经元的电刺激仅引起单个尖峰。如果我们现在将毒蕈碱添加到神经元中，毒蕈碱受体的激活会关闭超极化的 M 电流，从而导致小的去极化。如果我们在持续存在毒蕈碱的情况下重复电刺激（见图 14-9C），则会出现重复的尖峰，因为 M 电流稳定作用的丧失增加了神经元的兴奋性。毒蕈碱反应的缓慢调节作用大大增强了 ANS 控制内脏活动的能力，超出了仅使用快速烟碱 EPSP 所能完成的能力。

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