von Kügelgen I, Kurz K, Bültmann R, Driessen B, Starke K
Pharmakologisches Institut, Universität Freiburg, Germany.
Fundam Clin Pharmacol. 1994;8(3):207-13. doi: 10.1111/j.1472-8206.1994.tb00800.x.
The release of both sympathetic co-transmitters, noradrenaline and ATP, is modulated via presynaptic receptors. However, the degree of the modulation may differ indicating that the ratio of the released co-transmitters changes upon presynaptic receptor activation. For example, alpha 2-autoinhibition affects the release of noradrenaline more markedly than the release of ATP. Some sympathetic axon terminals possess presynaptic P2-purinoceptors which are activated by endogenous ATP. These receptors are a novel kind of auto-receptor: they mediate a presynaptic negative feedback mechanism in which released ATP inhibits subsequent co-transmitter release.
交感神经共同递质去甲肾上腺素和三磷酸腺苷（ATP）的释放均通过突触前受体进行调节。然而，调节程度可能不同，这表明释放的共同递质的比例在突触前受体激活时会发生变化。例如，α2-自身抑制对去甲肾上腺素释放的影响比对ATP释放的影响更为明显。一些交感神经轴突终末具有突触前P2-嘌呤受体，可被内源性ATP激活。这些受体是一种新型的自身受体：它们介导一种突触前负反馈机制，其中释放的ATP抑制随后的共同递质释放。
