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General anesthetics modulate GABA receptor channel complex in rat dorsal root ganglion neurons

The effects of halothane, isoflurane, and enflurane on ionic currents induced by bath application of γ‐aminobutyric acid (GABA) were studied with the rat dorsal root ganglion neurons maintained in primary culture. The whole‐cell patch clamp technique was used to record the current. In normal neurons before exposure to anesthetics, GABA at low concentrations (1‐3 times 10−6 M) induced a small sustained inward current. At higher concentrations (3 times 10−5 M‐1 times 10−3 M), GABA induced a large inward current, which decayed to a steady‐state level (desensitization). Halothane (0.86 mM), isoflurane (0.96 mM), and enflurane (1.89 mM), each equivalent to the respective 2 minimum alveolar concentration (MAC) units, augmented the sustained current evoked by 3 times 10−6 M GABA to 330‐350% of control and the peak current evoked by 3 times 10−5 M of GABA to 136‐145% of control. The decay phase of the current was accelerated by the anesthetics, the time for the current to decline to 70% of the peak being reduced to 23‐39% of control. In contrast, the desensitized steady‐state current evoked by high concentrations of GABA was decreased by anesthetics. In conclusion, general anesthetics exert a dual effect on the GABA receptor channel complex: to potentiate the nondesensitized (both peak and sustained) current and to suppress the desensitized steady‐state current. The potentiation of the GABA receptor channel response may be a primary action of anesthetics leading to surgical anesthesia.—Nakahiro, M.; Yeh, J. Z.; Brunner, E.; Narahashi, T. General anesthetics modulate GABA receptor channel complex in rat dorsal root ganglion neurons. FASEB J. 3: 1850‐1854; 1989.