Gähwiler B H, Dreifuss J J
Brain Res. 1980 Jul 14;193(2):415-25. doi: 10.1016/0006-8993(80)90174-2.
Intracellular recordings of the spontaneous activity were obtained from neurons in long-term cultures from the area of the supraoptic nucleus of rats. The effects of various substances known from in situ studies to cause vasopressin release were analyzed. Application of nicotine or acetylcholine induced a transition from a random to a phasic discharge pattern. Similar alterations in firing patterns were observed with enkephalin analogues, an effect which was blocked by the opiate antagonist, naloxone. Glutamate excited hypothalamic neurons in a dose-dependent manner, but did not induce phasic firing. Angiotensin II increased the firing rate in randomly firing cells and the duration of bursts in phasic cells. In an attempt to identify the transmitter(s) involved in the generation of phasic activity, several antagonists to excitatory transmitters were applied. Of the agents tested, only saralasin reduced the duration of bursts, but it is questionable whether this effect is due to its angiotensin-antagonistic property.
从大鼠视上核区域的长期培养神经元中获得了自发活动的细胞内记录。分析了原位研究中已知的各种引起血管加压素释放的物质的作用。应用尼古丁或乙酰胆碱可诱导从随机放电模式向相位放电模式的转变。脑啡肽类似物也观察到了类似的放电模式改变，这种效应被阿片拮抗剂纳洛酮阻断。谷氨酸以剂量依赖的方式兴奋下丘脑神经元，但不诱导相位放电。血管紧张素II增加了随机放电细胞的放电频率和相位细胞的爆发持续时间。为了确定参与相位活动产生的神经递质，应用了几种兴奋性神经递质拮抗剂。在测试的药物中，只有沙拉新减少了爆发的持续时间，但这种效应是否归因于其血管紧张素拮抗特性尚存在疑问。
