Fig. 2.
Direct activation of GABAA receptors by carisoprodol and meprobamate. A, representative traces demonstrating inward currents evoked by carisoprodol and meprobamate in the absence of GABA. B, current amplitude of carisoprodol- or meprobamate-evoked currents relative to currents evoked by 10 μM GABA. Each bar represents the mean ± S.E. of a minimum of three cells; ***, significant difference relative to an equal concentration of meprobamate (p < 0.001). C, representative traces of carisoprodol-mediated currents in the presence of various concentrations of PTX. Current amplitude was measured at the end of the 10-s coapplication period. D, summary of results illustrated in C; carisoprodol-activated currents were reduced to 45.7 ± 2.5% and 16.6 ± 4.3% of control in the presence of 30 and 100 μM PTX, respectively. Recovery from PTX was 78.7 ± 9.0% of control (data not shown). Antagonism by PTX suggests the carisoprodol-activated current was conducted via GABAA receptors. Each bar represents the mean ± S.E. of four cells.