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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Angiotensin II stimulates spinally projecting paraventricular neurons through presynaptic disinhibition.
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Angiotensin II stimulates spinally projecting paraventricular neurons through presynaptic disinhibition.

机译：血管紧张素II通过突触前抑制作用刺激脊柱投射的脑室旁神经元。

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摘要

Paraventricular nucleus (PVN) neurons that project to the spinal cord are important in the control of sympathetic outflow. Angiotensin II (Ang II) can stimulate PVN neurons, but its cellular mechanisms are not clear. In this study, we determined the effect of Ang II on the excitatory and inhibitory synaptic inputs to spinally projecting PVN neurons. Whole-cell patch-clamp recordings were performed on PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Immunocytochemistry labeling revealed that the immunoreactivity of angiotensin type 1 (AT1) receptors was colocalized with a presynaptic marker, synaptophysin, in the PVN. Application of 0.1-5 microm Ang II significantly decreased the amplitude of evoked GABAergic IPSCs in a concentration-dependent manner. Also, Ang II decreased the frequency of miniature IPSCs from 2.56 +/- 0.45 to 1.05 +/- 0.20 Hz (p < 0.05; n = 12), without affecting the amplitude and the decay time constant. The effect of Ang II on miniature IPSCs was blocked by losartan but not PD123319. However, Ang II had no effect on the evoked glutamatergic EPSCs and did not alter the frequency and amplitude of miniature EPSCs at concentrations that attenuated IPSCs. Furthermore, Ang II increased the firing rate of PVN neurons from 3.75 +/- 0.36 to 7.89 +/- 0.85 Hz (p < 0.05; n = 9), and such an effect was abolished by losartan. In addition, Ang II failed to excite PVN neurons in the presence of bicuculline. Thus, this study provides substantial new evidence that Ang II excites spinally projecting PVN neurons by attenuation of GABAergic synaptic inputs through activation of presynaptic AT1 receptors.
机译：突出到脊髓的脑室旁核（PVN）神经元在控制交感神经流出中很重要。血管紧张素II（Ang II）可以刺激PVN神经元，但其细胞机制尚不清楚。在这项研究中，我们确定了Ang II对脊髓投射PVN神经元的兴奋性和抑制性突触输入的影响。全细胞膜片钳记录是在PVN神经元上进行的，该神经元由注入大鼠胸脊髓的逆行荧光示踪剂标记。免疫细胞化学标记显示，血管紧张素1型（AT1）受体的免疫反应性与突触前标记突触素在PVN中共定位。 0.1-5微米Ang II的应用以浓度依赖的方式显着降低了诱发的GABA能IPSC的幅度。同样，Ang II将微型IPSC的频率从2.56 +/- 0.45降低到1.05 +/- 0.20 Hz（p <0.05; n = 12），而不会影响幅度和衰减时间常数。氯沙坦可阻断Ang II对微型IPSC的作用，但PD123319不能。但是，Ang II对诱发的谷氨酸能EPSC没有影响，并且在减弱IPSC的浓度下也不会改变微型EPSC的频率和幅度。此外，Ang II将PVN神经元的放电频率从3.75 +/- 0.36 Hz增加到7.89 +/- 0.85 Hz（p <0.05; n = 9），氯沙坦取消了这种作用。此外，在存在双小分子的情况下，Ang II未能激发PVN神经元。因此，这项研究提供了实质性的新证据，即Ang II通过激活突触前AT1受体而减弱GABA能突触输入，从而激发脊髓投射PVN神经元。

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