Fig. 4. Propofol toxicity is not mediated by γ-aminobutyric acid type A (GABAA) receptor activation. Neural precursor cells in proliferation media were exposed to propofol in the presence or absence of the GABAAreceptor antagonists bicuculline or picrotoxin. Six hours of 14.3 µM (A ) or 71.4 µM (B ) propofol induced lactate dehydrogenase (LDH) release that was not inhibited by addition of bicuculline. Similarly, the channel blocker picrotoxin did not block LDH release after propofol exposure for 6 h (C ). Treating neural precursor cells with GABAAreceptor agonists midazolam (D ) or muscimol (E ) did not cause release of LDH from neural precursor cells over a wide range of concentrations (Bonferroni correction vs. control or treatment pair). **P < 0.01, ***P < 0.001. DMSO = dimethyl sulfoxide; LDH = lactate dehydrogenase; NS = not significant.