The Actions of Propofol on γ-Aminobutyric Acid-A and Glycine Receptors in Acutely Dissociated Spinal Dorsal Horn Neurons of the Rat

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Abstract
The spinal cord plays an important role in modulating anesthetic-induced suppression of nociceptive transmission. To gain some insight into the anesthetic mechanisms of propofol at the spinal level, we investigated the direct action of propofol and its modulation on the gamma-aminobutyric acid-A receptor (GABA(A)R) and the glycine receptor (GlyR) in acutely dissociated rat spinal dorsal horn neurons by using whole-cell patch-clamp electrophysiology. Propofol induced Cl(-) currents (I(Cl)), which were sensitive to bicuculline and, to a lesser extent, to strychnine. The activation, desensitization, and deactivation of propofol-induced I(Cl) were slower than those of GABA- and glycine-induced I(Cl). In addition, this study revealed similar modulatory actions of propofol on GABA(A)R and GlyR. Propofol potentiated both GABA- and glycine-induced I(Cl) at small con-centrations and inhibited both GABA- and glycine-induced I(Cl) at large concentrations. The potentiation of propofol on I(Cl) was caused by slowing current desensitization and deactivation, whereas the inhibition actions might be involved in the cross-desensitization between GABA- and propofol-induced I(Cl) and the cross-inhibition between the GABA(A)R and GlyR. The results suggest that propofol facilitation of GABA(A)R and GlyR at the spinal level could contribute significantly to general anesthetic-induced analgesia and anesthesia. The actions of propofol on the gamma-aminobutyric acid-A receptor (GABA(A)R) and the glycine receptor (GlyR) were investigated in acutely dissociated rat spinal dorsal horn neurons by using whole-cell patch-clamp electrophysiology. Propofol was found to potentiate the functions of GABA(A)R and GlyR at the spinal level, which might contribute to propofol-induced analgesia and anesthesia.