Khanna S, Sibbald J R, Day T A
Department of Physiology and Pharmacology, University of Queensland, Australia.
Brain Res. 1993 Jun 4;613(1):164-7. doi: 10.1016/0006-8993(93)90469-4.
The A1 noradrenaline (NA) cell group of the caudal medulla provides a direct excitatory input to supraoptic nucleus (SON) vasopressin (VP) cells. We have now investigated the possibility that NA released from A1 terminals acts presynaptically to modulate A1 input to VP cells. Initial experiments done in pentobarbitone anaesthetized rats established that SON application of NA excited VP cells but also depressed their response to activation of the A1 input. Moreover, the latter effect was mimicked by the alpha 2-adrenoceptor agonist clonidine and antagonised by intravenous administration of the alpha 2-adrenoceptor antagonist yohimbine. Further studies showed that yohimbine also prevented the relative decline in synaptic excitation of VP cells normally observed as A1 activation frequency increases. These data are consistent with the proposal that NA, released from the SON terminals of A1 NA cells, acts via alpha 2-adrenoceptors to depress A1 transmitter release and thus A1 influence on VP cells.
延髓尾部的A1去甲肾上腺素(NA)细胞群为视上核(SON)的血管加压素(VP)细胞提供直接的兴奋性输入。我们现在研究了从A1终末释放的NA是否通过突触前作用来调节A1对VP细胞的输入。在戊巴比妥麻醉的大鼠中进行的初步实验表明,向SON施加NA可兴奋VP细胞,但也会抑制它们对A1输入激活的反应。此外,α2肾上腺素能受体激动剂可乐定可模拟后一种效应,而静脉注射α2肾上腺素能受体拮抗剂育亨宾可拮抗该效应。进一步的研究表明,育亨宾还可阻止通常在A1激活频率增加时观察到的VP细胞突触兴奋的相对下降。这些数据与以下观点一致:从A1 NA细胞的SON终末释放的NA通过α2肾上腺素能受体发挥作用,抑制A1递质释放,从而抑制A1对VP细胞的影响。