Skip to main content
. 2009 Feb 24;329(2):827–837. doi: 10.1124/jpet.109.151142

Fig. 2.

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.