Akaishi T, Negoro H, Kobayasi S
Brain Res. 1980 Apr 28;188(2):499-511. doi: 10.1016/0006-8993(80)90048-7.
Extracellular recordings of action potentials were made from neurones antidromically identified as neurosecretory cells in the paraventricular and supraoptic nuclei of urethane-anesthetized female rats. Eighty-six neurones were examined for their responsiveness to 10 ng of angiotensin II (AII) injected into the third cerebral ventricle and 78 (91%) of them increased their firing rate following the AII injection. None of the neurosecretory cells tested showed a response to the intraventricular (IVT) injection of isotonic NaCl. Thalamic neurones and non-neurosecretory hypothalamic neurones did not respond to the AII given IVT. Firing activity of 13 neurosecretory neurones was recorded during reflex milk ejection induced by suckling pups in the lactating rats. Seven of them were classified as oxytocinergic cells because they showed a burst of activity before reflex milk ejections and the remaining 6 neurones which gave no burst of firing before milk ejections were classified as nonoxytocinergic neurones. The IVT application of AII resulted in activation of all the oxytocinergic neurones and 5 of the 6 non-oxytocinergic neurones. The effect of AII on the firing of the neurosecretory cell was inhibited by the simultaneous application of Sar1-Ile8-AII (1 microgram), a competitive AII antagonist. The IVT injection of the antagonist alone inhibited the spontaneous firing of the neurosecretory cells, but it did not affect the firing of thalamic or non-neurosecretory hypothalamic neurones. Hypertonic NaCl (0.85 M NaCl, 1 mu1 IVT) also activated 13 of 20 neurosecretory cells tested. Combined application of AII and hypertonic NaCl elicited a marked potentiation of the response of neurosecretory cells to each of the stimuli. These findings indicate that AII activates neurosecretory cells stimulating specific AII receptors in the brain and that AII has a synergistic action with hypertonic NaCl. Inhibition of spontaneous activity of neurosecretory cells by a competitive AII antagonist suggests that endogenous AII may participate in the maintenance of basal activity of neurosecretory cells.
在氨基甲酸乙酯麻醉的雌性大鼠的室旁核和视上核中,对经逆向鉴定为神经分泌细胞的神经元进行动作电位的细胞外记录。检测了86个神经元对注入第三脑室的10纳克血管紧张素II(AII)的反应性,其中78个(91%)在注入AII后 firing rate增加。所测试的神经分泌细胞中没有一个对脑室内(IVT)注入等渗氯化钠有反应。丘脑神经元和非神经分泌性下丘脑神经元对IVT给予的AII无反应。在哺乳大鼠中,记录了13个神经分泌神经元在幼崽吸吮诱导的反射性乳汁排出过程中的放电活动。其中7个被归类为催产素能细胞,因为它们在反射性乳汁排出前出现一阵活动,其余6个在乳汁排出前没有一阵放电的神经元被归类为非催产素能神经元。IVT应用AII导致所有催产素能神经元和6个非催产素能神经元中的5个被激活。同时应用Sar1-Ile8-AII(1微克),一种竞争性AII拮抗剂,可抑制AII对神经分泌细胞放电的影响。单独IVT注射拮抗剂可抑制神经分泌细胞的自发放电,但不影响丘脑或非神经分泌性下丘脑神经元的放电。高渗氯化钠(0.85 M NaCl,1微升IVT)也激活了所测试的20个神经分泌细胞中的13个。联合应用AII和高渗氯化钠可显著增强神经分泌细胞对每种刺激的反应。这些发现表明,AII通过刺激脑中特定的AII受体激活神经分泌细胞,并且AII与高渗氯化钠具有协同作用。竞争性AII拮抗剂对神经分泌细胞自发放电的抑制表明内源性AII可能参与神经分泌细胞基础活动的维持。