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. (4th July 2017)
- Record Type:
- Journal Article
- Title:
- 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. (4th July 2017)
- Main Title:
- 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
- Authors:
- Guo, Yuhong
Yan, Xianxia
Chen, Xingxin
He, Ding
Zeng, Ming
Chen, Yonghua
Xia, Chunmei
Qiu, Dongying
Wang, Jijiang - Abstract:
- Highlights: Corticotropin-releasing hormone depolarized airway vagal preganglionic neuron (AVPN). Corticotropin-releasing hormone caused a tonic excitatory current in AVPN. Corticotropin-releasing hormone enhanced the glutamatergic synaptic inputs of AVPN. Corticotropin-releasing hormone enhanced the GABAergic synaptic inputs of AVPN. Type 1 receptor antagonist blocked the effects of corticotropin-releasing hormone. Abstract: Corticotropin-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 (200 nmol L −1 ) were examined using whole-cell patch clamp. The results show that under current clamp, corticotropin-releasing hormone (200 nmol L −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 (1 μmol L −1 ), corticotropin-releasing hormone had no impact on the miniatureHighlights: Corticotropin-releasing hormone depolarized airway vagal preganglionic neuron (AVPN). Corticotropin-releasing hormone caused a tonic excitatory current in AVPN. Corticotropin-releasing hormone enhanced the glutamatergic synaptic inputs of AVPN. Corticotropin-releasing hormone enhanced the GABAergic synaptic inputs of AVPN. Type 1 receptor antagonist blocked the effects of corticotropin-releasing hormone. Abstract: Corticotropin-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 (200 nmol L −1 ) were examined using whole-cell patch clamp. The results show that under current clamp, corticotropin-releasing hormone (200 nmol L −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 (1 μmol L −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 (50 μmol L −1 ), an antagonist of type 1 corticotropin-releasing hormone receptors, but insensitive to Astressin 2B (200 nmol L −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. … (more)
- Is Part Of:
- Neuroscience. Volume 355(2017)
- Journal:
- Neuroscience
- Issue:
- Volume 355(2017)
- Issue Display:
- Volume 355, Issue 2017 (2017)
- Year:
- 2017
- Volume:
- 355
- Issue:
- 2017
- Issue Sort Value:
- 2017-0355-2017-0000
- Page Start:
- 101
- Page End:
- 112
- Publication Date:
- 2017-07-04
- Subjects:
- aCSF artificial cerebral spinal fluid -- AHR airway hyperreactivity -- Antalarmin hydrochloride N-Butyl-N-ethyl-2, 5, 6-trimethyl-7-(2, 4, 6-trimethylphenyl)-7H-pyrrolo[2, 3-d]pyrimidin-4-amine hydrochloride -- AP5 D-2-amino-5-phosphonovalerate -- AVPNs airway vagal preganglionic neurons -- CNQX 6-Cyano-7-nitroquinoxaline-2, 3-dione -- CRH corticotropin-releasing hormone -- DMNV dorsal motor nucleus of the vagus -- eNA the external formation of the nucleus ambiguus -- HPA hypothalamic-pituitary-adrenocortical -- IA-AVPNs inspiratory-activated airway vagal preganglionic neurons -- II-AVPNs inspiratory-inhibited airway vagal preganglionic neurons -- mEPSCs miniature excitatory postsynaptic currents -- mIPSCs miniature inhibitory postsynaptic currents -- NA nucleus ambiguus -- sEPSCs spontaneous excitatory postsynaptic currents -- sIPSCs spontaneous inhibitory postsynaptic currents -- TTX tetrodotoxin
airway -- corticotrophin-releasing hormone -- preganglionic -- synapse -- vagus
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612.8 - Journal URLs:
- http://www.sciencedirect.com/science/journal/03064522 ↗
http://www.clinicalkey.com/dura/browse/journalIssue/03064522 ↗
http://www.clinicalkey.com.au/dura/browse/journalIssue/03064522 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.neuroscience.2017.04.049 ↗
- Languages:
- English
- ISSNs:
- 0306-4522
- Deposit Type:
- Legaldeposit
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