Tanaka J, Nojima K, Yamamuro Y, Saito H, Nomura M
Department of Physiology, Saitama Medical School, Japan.
Brain Res. 1993 Apr 9;608(1):141-4. doi: 10.1016/0006-8993(93)90785-l.
The activity of subfornical organ (SFO) neurons that were antidromically identified by electrical stimulation of the rat hypothalamic paraventricular nucleus (PVN) was tested for a response to microiontophoretic application of angiotensin II (ANG II) or hemorrhage (10 ml/kg b.w.t.). Microiontophoretically (MIPh) applied ANG II caused an increased excitability in 24 out of 28 neurons tested and the excitation was blocked by MIPh-applied saralasin (Sar), a specific ANG II antagonist. Of these neurons that responded to ANG II, 14 displayed an increase in neuronal firing in response to hemorrhage, while 10 were unresponsive. The excitatory response to hemorrhage in 5 out of 14 neurons tested was prevented by MIPh-applied Sar, whereas the response of the remaining neurons was not affected. These results show that part of SFO neurons projecting to the PVN may receive neural inputs from the peripheral baroreceptors, and suggest that the inputs may be partially attributable to the involvement of central angiotensinergic circuits.
通过电刺激大鼠下丘脑室旁核（PVN）逆向鉴定的穹窿下器官（SFO）神经元，检测其对微量离子导入血管紧张素II（ANG II）或出血（10 ml/kg体重）的反应。微量离子导入（MIPh）施加的ANG II使28个受试神经元中的24个兴奋性增加，且这种兴奋被MIPh施加的沙拉新（Sar）阻断，沙拉新是一种特异性ANG II拮抗剂。在这些对ANG II有反应的神经元中，14个对出血有神经元放电增加反应，而10个无反应。在14个受试神经元中，5个对出血的兴奋反应被MIPh施加的Sar阻断，而其余神经元的反应未受影响。这些结果表明，投射到PVN的部分SFO神经元可能接受来自外周压力感受器的神经输入，并提示这些输入可能部分归因于中枢血管紧张素能回路的参与。
