• Neuroscience · Jul 2017

    Corticotropin-releasing hormone modulates airway vagal preganglionic neurons of Sprague-Dawley rats at multiple synaptic sites via activation of its type 1 receptors: implications for stress-associated airway vagal excitation.

    • Yuhong Guo, Xianxia Yan, Xingxin Chen, Ding He, Ming Zeng, Yonghua Chen, Chunmei Xia, Dongying Qiu, and Jijiang Wang.
    • Department of Neurobiology, School of Basic Medical Sciences, Fudan University, China.
    • Neuroscience. 2017 Jul 4; 355: 101112101-112.

    AbstractCorticotropin-releasing hormone release is the final common pathway of stress-associated neuroendocrine responses. This study tested how corticotropin-releasing hormone modulates airway vagal preganglionic neurons. Airway vagal preganglionic neurons in neonatal rats were retrogradely labeled with fluorescent dye and identified in medullary slices, and their responses to corticotropin-releasing hormone (200nmolL-1) were examined using whole-cell patch clamp. The results show that under current clamp, corticotropin-releasing hormone (200nmolL-1) depolarized airway vagal preganglionic neurons and significantly increased the rate of their spontaneous firing. Under voltage clamp, corticotropin-releasing hormone caused a tonic inward current and significantly facilitated the spontaneous glutamatergic and GABAergic inputs of these neurons. Corticotropin-releasing hormone had no impact on the spontaneous glycinergic inputs of these neurons. In the preexistence of tetrodotoxin (1μmolL-1), corticotropin-releasing hormone had no impact on the miniature excitatory or inhibitory postsynaptic currents, but still induced a tonic inward current and significantly increased the input resistance. The responses induced by corticotropin-releasing hormone were prevented by Antalarmin hydrochloride (50μmolL-1), an antagonist of type 1 corticotropin-releasing hormone receptors, but insensitive to Astressin 2B (200nmolL-1), an antagonist of type 2 corticotropin-releasing hormone receptors. These results suggest that corticotropin-releasing hormone excites airway vagal preganglionic neurons via activation of its type 1 receptors at multiple sites, which includes a direct postsynaptic excitatory action and presynaptic facilitation of both glutamatergic and GABAergic inputs. In stress, corticotropin-releasing hormone might be able to activate the airway vagal nerves and, consequently, participate in induction or exacerbation of airway disorders.Copyright © 2017 IBRO. Published by Elsevier Ltd. All rights reserved.

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