• Esperanza Recio-Pinto, Jose V Montoya-Gacharna, Fang Xu, and BlanckThomas J JTJJ.
• From the Department of Anesthesiology, NYU Langone Medical Center, New York, New York.
• Anesth. Analg. 2016 Mar 1; 122 (3): 730-737.

BackgroundVolatile anesthetics decrease Ca²⁺ entry through voltage-dependent Ca²⁺ channels. Ca influences neurotransmitter release and neuronal excitability. Because volatile anesthetics act specifically on the spinal cord to produce immobility, we examined the effect of isoflurane and the nonimmobilizers F6 (1, 2-dichlorohexafluorocyclobutane) and F8 (2, 3-dichlorooctafluorobutane) on CaV1 and CaV2 Ca²⁺ channels in spinal cord motor neurons and dorsal root ganglion neurons.MethodsUsing patch clamping, we compared the effects of isoflurane with those of F6 and F8 on CaV1 and CaV2 channels in isolated, cultured adult rat spinal cord motor neurons and on CaV1 and CaV2 channels in adult rat dorsal root ganglion sensory neurons.ResultsIn spinal cord motor neurons, isoflurane, but not F6 or F8, inhibited currents through CaV1 channels. Isoflurane and at least one of the nonimmobilizers inhibited currents through CaV1 and CaV2 channels in dorsal root ganglion neurons and CaV2 in spinal cord motor neurons.ConclusionsThe findings that isoflurane, but not nonimmobilizers, inhibited CaV1 Ca²⁺ channels in spinal cord motor neurons are consistent with the notion that spinal cord motor neurons might mediate isoflurane-induced immobility. Additional studies are required to examine whether inhibition of CaV1 calcium currents in spinal cord motor neurons is sufficient or whether actions on other channels/proteins contribute to isoflurane-induced immobility.

34 keywords...

hide…