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首页> 外文期刊>Journal of Neurophysiology >Regulation of synaptic inputs to paraventricular-spinal output neurons by alpha2 adrenergic receptors.
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Regulation of synaptic inputs to paraventricular-spinal output neurons by alpha2 adrenergic receptors.

机译：α2肾上腺素能受体对脑室旁输出神经元的突触输入的调节。

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摘要

Neurons in the paraventricular nucleus (PVN) that project to the brain stem and spinal cord are important for autonomic regulation. The excitability of preautonomic PVN neurons is controlled by the noradrenergic input from the brain stem. In this study, we determined the role of alpha(2) adrenergic receptors in the regulation of excitatory and inhibitory synaptic inputs to spinally projecting PVN neurons. Excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs) were recorded using whole cell voltage-clamp techniques on PVN neurons labeled by a retrograde fluorescence tracer injected into the thoracic spinal cord of rats. Bath application of 5-20 muM clonidine, an alpha(2) receptor agonist, significantly reduced the amplitude of evoked GABAergic IPSCs in a dose-dependent manner. Also, 10 microM clonidine significantly decreased the frequency (from 2.68 +/- 0.41 to 1.22 +/- 0.40 Hz) but not the amplitude of miniature IPSCs (mIPSCs), and this effect was blocked by the alpha(2) receptor antagonistyohimbine. Furthermore, clonidine increased the paired-pulse ratio of evoked IPSCs from 1.25 +/- 0.05 to 1.61 +/- 0.08 (P < 0.05). On the other hand, clonidine had little effect on evoked glutamatergic EPSCs, mEPSCs, and the paired-pulse ratio of evoked EPSCs in most labeled cells examined. Additionally, immunofluorescence labeling revealed that the alpha(2A) receptor and GABA immunoreactivities were co-localized in close apposition to labeled PVN neurons. Collectively, these data suggest that stimulation of alpha(2) adrenergic receptors primarily attenuates GABAergic inputs to PVN output neurons to the spinal cord. The presynaptic alpha(2) receptors function as heteroreceptors to modulate synaptic GABA release and contribute to the hypothalamic regulation of sympathetic outflow.
机译：突出到脑干和脊髓的室旁核（PVN）中的神经元对于自主调节很重要。前自主神经PVN神经元的兴奋性由脑干的去甲肾上腺素输入控制。在这项研究中，我们确定了α（2）肾上腺素能受体在脊突投射PVN神经元的兴奋性和抑制性突触输入调节中的作用。使用全细胞电压钳技术在通过注入大鼠胸脊髓的逆行荧光示踪剂标记的PVN神经元上记录兴奋性和抑制性突触后电流（EPSC和IPSC）。洗澡应用5-20μM可乐定，一种α（2）受体激动剂，以剂量依赖性方式显着降低了诱发的GABA能IPSC的幅度。同样，10 microM可乐定可显着降低频率（从2.68 +/- 0.41降低至1.22 +/- 0.40 Hz），但不会降低微型IPSC（mIPSC）的幅度，并且这种作用被alpha（2）受体拮抗剂育亨宾所阻断。此外，可乐定将诱发的IPSC的配对脉冲比从1.25 +/- 0.05增加到1.61 +/- 0.08（P <0.05）。另一方面，可乐定在大多数检查的标记细胞中对诱发的谷氨酸能EPSC，mEPSC和诱发的EPSC的成对脉冲比影响很小。此外，免疫荧光标记显示，α（2A）受体和GABA免疫反应性共定位于与标记的PVN神经元紧密相邻的位置。总的来说，这些数据表明，对α（2）肾上腺素能受体的刺激主要减弱了GABA能输入到脊髓的PVN输出神经元的能力。突触前的alpha（2）受体作为异受体来调节突触GABA的释放，并有助于下丘脑调节交感神经的流出。

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