THYROTROPIN-RELEASING HORMONE CAUSES A TONIC EXCITATORY POSTSYNAPTIC CURRENT AND INHIBITS THE PHASIC INSPIRATORY INHIBITORY INPUTS IN INSPIRATORY-INHIBITED AIRWAY VAGAL PREGANGLIONIC NEURONS
THYROTROPIN-RELEASING HORMONE CAUSES A TONIC EXCITATORY POSTSYNAPTIC CURRENT AND INHIBITS THE PHASIC INSPIRATORY INHIBITORY INPUTS IN INSPIRATORY-INHIBITED AIRWAY VAGAL PREGANGLIONIC NEURONS
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促甲状腺素释放激素引起强直性兴奋性突触后电流，并抑制吸气抑制气道迷走神经节前神经元的阶段性吸气抑制输入
DOI：
10.1016/j.neuroscience.2011.12.003
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发表时间：
2012-01-27
期刊：
影响因子：
3.3
通讯作者：
Wang, J.
中科院分区：
文献类型：
--
作者：
Hou, L.;Zhou, X.;Wang, J.
疑核（eNA）外部结构中的气道迷走神经节前神经元（AVPNs）包括吸气激活的AVPNs（IA-AVPNs）和吸气抑制的AVPNs（II-AVPNs），在气管和支气管的控制中占主导地位。AVPN从含有促甲状腺激素释放激素（TRH）的终端接收特别密集的输入。疑核内微量注射TRH引起气管平滑肌收缩。然而，目前尚不清楚TRH是否影响eNA中所有亚型的AVPN，并因此影响气道中所有类型的靶组织（平滑肌、粘膜下腺体和血管）的控制。TRH如何在神经元和突触水平影响AVPN也是未知的。在这项研究中，在eNA的AVPNs逆行标记从胸外气管，II-AVPNs被确定在节律性放电的脑干切片，TRH的作用进行了检查，使用膜片钳。TRH（100 nmol L ~（-1））可增强舌下神经爆发的节律和强度，并在保持电压为-80 mV时在II-AVPN内引起紧张性兴奋性内向电流。自发兴奋性突触后电流（EPSC）的频率在II-AVPNs，这表明在一个呼吸周期中，没有相关的变化，没有显着改变TRH。在保持电压为-50 mV时，II-AVPN显示自发和阶段性吸气（外向）抑制性突触后电流（IPSC）。TRH对自发性IPSC无影响，但显著减弱相性吸气外向电流的幅度和面积。局部应用甘氨酸受体拮抗剂士的宁后，自发的IPSC非常稀少，相性吸气抑制电流被取消;进一步应用TRH对这些电流没有影响。在电流钳模式下，TRH引起吸气间期II-AVPNs的去极化和放电频率增加。这些结果表明，TRH影响的II-AVPNs突触后通过直接的兴奋性电流和突触前通过衰减的相位甘氨酸能突触输入。(C)2011年IBRO。由爱思唯尔有限公司出版。保留所有权利。
The airway vagal preganglionic neurons (AVPNs) in the external formation of the nucleus ambiguus (eNA), which include the inspiratory-activated AVPNs (IA-AVPNs) and inspiratory-inhibited AVPNs (II-AVPNs), predominate in the control of the trachea and bronchia. The AVPNs receive particularly dense inputs from terminals containing thyrotropin-releasing hormone (TRH). TRH microinjection into the nucleus ambiguus (NA) caused constriction of the tracheal smooth muscles. However, it is unknown whether TRH affects all subtypes of the AVPNs in the eNA, and as a result affects the control of all types of target tissues in the airway (smooth muscles, submucosal glands, and blood vessels). It is also unknown how TRH affects the AVPNs at neuronal and synaptic levels. In this study, the AVPNs in the eNA were retrogradely labeled from the extrathoracic trachea, the II-AVPNs were identified in rhythmically firing brainstem slices, and the effects of TRH were examined using patch-clamp. TRH (100 nmol L-1) enhanced both the rhythm and the intensity of the hypoglossal bursts, and caused a tonic excitatory inward current in the II-AVPNs at a holding voltage of -80 mV. The frequency of the spontaneous excitatory postsynaptic currents (EPSCs) in the II-AVPNs, which showed no respiratory-related change in a respiratory cycle, was not significantly changed by TRH. At a holding voltage of -50 mV, the II-AVPNs showed both spontaneous and phasic inspiratory (outward) inhibitory postsynaptic currents (IPSCs). TRH had no effect on the spontaneous IPSCs but significantly attenuated the phasic inspiratory outward currents, in both the amplitude and area. After focal application of strychnine, an antagonist of glycine receptors, to the II-AVPNs, the spontaneous IPSCs were extremely scarce and the phasic inspiratory inhibitory currents were abolished; and further application of TRH had no effect on these currents. Under current clamp configuration, TRH caused a depolarization and increased the firing rate of the II-AVPNs during inspiratory intervals. These results demonstrate that TRH affects the II-AVPNs both postsynaptically via a direct excitatory current and presynaptically via attenuation of the phasic glycinergic synaptic inputs. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.