Abstract PR430

Abstract

Background & Objectives: Although accumulative evidence indicates the thalamocortical system is an important target for general anesthetics, the underlying mechanisms of anesthetic action on thalamocortical neurotransmission are not fully understood. The aim of the study is to explore the action of etomidate on glutamatergic and GABAergic transmission in rat thalamocortical slices by using whole cell patch-clamp recording technique. Materials & Methods: Spontaneous glutamatergic excitatory postsynaptic currents and GABAergic inhibitory postsynaptic currents were recorded from rat thalamocortical slices by using whole cell patch-clamp recording technique. Results: In thalamocortical neurons, we found that etomidate decreased the frequency of spontaneous glutamatergic excitatory postsynaptic currents (sEPSCs) without affecting the amplitude and decay time, which suggests that etomidate decreases glutamatergic transmission mainly through presynaptic acton. On the other hand, etomidate does-dependently prolonged the decay time of spontaneous GABAergic inhibitory postsynaptic currents (sIPSCs) without altering the frequency, which suggests facilitates GABAergic transmission through postsynaptic mechanism. Furthermore, we also observed the different effects of etomidate on the frequency of sEPSCs in the presence and absence of GABAA receptor antagonist. Etomidate decreased the frequency of sEPSCs in a concentration-dependent manner in the absence of GABAA receptors antagonist,but the inhibition effects on sEPSCs frequency of etomidate significantly decreased after blocking GABAA receptors using bicuculline. Conclusion: It appears that presynaptic GABAA receptors activation is required for etomidate-induced decreases of presynaptic glutamate release. We speculate that the different action of etomidate on glutamatergic and GABAergic transmission may modulate the process of etomidate-induced loss of consciousness. Disclosure of Interest: None declared