Boehm S, Huck S
Department of Neuropharmacology, University of Vienna, Austria.
Prog Neurobiol. 1997 Feb;51(3):225-42. doi: 10.1016/s0301-0082(96)00056-1.
Primary cultures of postganglionic sympathetic neurons were established more than 30 years ago. More recently, these cultures have been used to characterize various neurotransmitter receptors that govern sympathetic transmitter release. These receptors may be categorized into at least three groups: (1) receptors which evoke transmitter release: (2) receptors which facilitate; (3) receptors which inhibit, depolarization-evoked release. Group (1) comprises nicotinic and muscarinic acetylcholine receptors, P2X purinoceptors and pyrimidinoceptors. Group (2) currently harbours beta-adrenoceptors, P2 purinoceptors, receptors for PACAP and VIP, as well as prostanoid EP1 receptors. In group (3), muscarinic cholinoceptors, alpha 2- and beta-adrenoceptors, P2 purinoceptors, and receptors for the neuropeptides NPY, somatostatin (SRIF1) and LHRH, as well as opioid (delta and kappa) receptors can be found. Receptors which regulate transmitter release from neurons in cell culture may be located either at the somatodendritic region or at the sites of exocytosis, i.e. the presynaptic specializations of axons. Most of the receptors that evoke release are located at the soma. There ionotropic receptors cause depolarizations to generate action potentials which then trigger Ca(2+)-dependent exocytosis at axon terminals. The signalling mechanisms of metabotropic receptors which evoke release still remain to be identified. Receptors which facilitate depolarization-evoked release appear to be located preferentially at presynaptic sites and presumably act via an increase in cyclic AMP. Receptors which inhibit stimulation evoked release are also presynaptic origin and most commonly rely on a G protein-mediated blockade of voltage-gated Ca2+ channels. Results obtained with primary cell cultures of postganglionic sympathetic neurons have now supplemented previous data about neurotransmitter receptors involved in the regulation of ganglionic as well as sympatho-effector transmission. In the future, this technique may prove useful to identify yet unrecognized receptors which control the output of the sympathetic nervous system and to elucidate underlying signalling mechanisms.
节后交感神经元的原代培养早在30多年前就已建立。最近，这些培养物已被用于表征控制交感递质释放的各种神经递质受体。这些受体至少可分为三类：（1）引发递质释放的受体；（2）促进释放的受体；（3）抑制去极化诱发释放的受体。第一类包括烟碱型和毒蕈碱型乙酰胆碱受体、P2X嘌呤受体和嘧啶受体。第二类目前包括β-肾上腺素能受体、P2嘌呤受体、PACAP和VIP受体以及前列腺素EP1受体。在第三类中，可以找到毒蕈碱型胆碱能受体、α2-和β-肾上腺素能受体、P2嘌呤受体以及神经肽NPY、生长抑素（SRIF1）和LHRH的受体，以及阿片样物质（δ和κ）受体。调节细胞培养中神经元递质释放的受体可能位于胞体树突区域或胞吐部位，即轴突的突触前特化部位。大多数引发释放的受体位于胞体。这些离子otropic受体引起去极化以产生动作电位，然后触发轴突末端的Ca(2+)依赖性胞吐作用。引发释放的代谢型受体的信号传导机制仍有待确定。促进去极化诱发释放的受体似乎优先位于突触前部位，大概是通过增加环磷酸腺苷起作用。抑制刺激诱发释放的受体也起源于突触前，最常见的是依赖G蛋白介导的电压门控Ca2+通道阻断。节后交感神经元原代细胞培养获得的结果现已补充了先前关于参与神经节以及交感效应器传递调节的神经递质受体的数据。未来，这项技术可能被证明有助于识别尚未被认识的控制交感神经系统输出的受体，并阐明潜在的信号传导机制。
