Dexmedetomidine decreases inhibitory but not excitatory neurotransmission to cardiac vagal neurons in the nucleus ambiguus
Document Type
Journal Article
Publication Date
1-1-2014
Journal
Brain Research
Volume
1574
DOI
10.1016/j.brainres.2014.06.010
Keywords
Cardiac vagal neuron; Dexmedetomidine; Inhibitory; Neurotransmission
Abstract
© 2014 Elsevier B.V. All rights reserved. Dexmedetomidine, an α2 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.
APA Citation
Sharp, D., Wang, X., & Mendelowitz, D. (2014). Dexmedetomidine decreases inhibitory but not excitatory neurotransmission to cardiac vagal neurons in the nucleus ambiguus. Brain Research, 1574 (). http://dx.doi.org/10.1016/j.brainres.2014.06.010