Dexmedetomidine decreases inhibitory but not excitatory neurotransmission to cardiac vagal neurons in the nucleus ambiguus

被引：23

作者：

Sharp, Douglas B. ^{[1
]}

Wang, Xin ^{[2
]}

Mendelowitz, David ^{[2
]}

机构：

[1] George Washington Univ, Dept Anesthesiol & Crit Care Med, Washington, DC 20037 USA

[2] George Washington Univ, Dept Physiol & Pharmacol, Washington, DC 20037 USA

来源：

BRAIN RESEARCH | 2014年 / 1574卷

关键词：

Dexmedetomidine; Cardiac vagal neuron; Inhibitory; Neurotransmission; GLUTAMATE RELEASE; CHILDREN;

D O I：

10.1016/j.brainres.2014.06.010

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Dexmedetomidine, an alpha(2) adrenergic agonist, is a useful sedative but can also cause significant bradycardia. This decrease in heart rate may be due to decreased central, sympathetic output as well as increased parasympathetic output from brainstem cardiac vagal neurons. In this study, using whole cell voltage clamp methodology, the actions of dexmedetomidine on excitatory glutamatergic and inhibitory GABAergic and glycinergic neurotransmission to parasympathetic cardiac vagal neurons in the rat nucleus ambiguus was determined. The results indicate that dexmedetomidine decreases both GABAergic and glycinergic inhibitory input to cardiac vagal neurons, with no significant effect on excitatory input. These results provide a mechanism for dexmedetomidine induced bradycardia and has implications for the management of this potentially harmful side effect. (C) 2014 Elsevier B.V. All rights reserved.

引用

页码：1 / 5

页数：5