Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons
Nicotine enhances both excitatory and inhibitory synaptic inputs to inspiratory‐activated airway vagal preganglionic neurons
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DOI:
10.1113/expphysiol.2012.066589
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发表时间:
2013-01
影响因子:
2.7
通讯作者:
Xujiao Zhou;Yonghua Chen;D. Ge;W. Yuan;Jijiang Wang
中科院分区:
文献类型:
--
作者:
Xujiao Zhou;Yonghua Chen;D. Ge;W. Yuan;Jijiang Wang
• What is the central question of this study? Airway vagal preganglionic neurons (AVPNs) supply the essential excitatory drive to the postganglionic neurons, which dominate the neural control of the airway physiologically and play critical roles in the pathogenesis of some common airway disorders. AVPNs express multiple subunits of nicotinic acetylcholine receptors (nAChRs), but the influences of exogenous nicotine or endogenous acetylcholine are unknown. • What is the main finding and its importance? Nicotine and endogenous acetylcholine both cause a postsynaptic excitatory current in inspiratory‐ activated AVPNs, and enhance both the excitatory and inhibitory synaptic inputs. The overall effect of nicotine on inspiratory‐activated AVPNs is excitatory. The nicotinic effects on inspiratory‐activated AVPNs are mediated presynaptically by activation of α4β2 type of nAChRs and postsynaptically by activation of multiple nAChRs including α7 and α4β2 types.