Fig. 2.
A γ aminobutyric acid A receptor inhibitor suppressed the propofol- or thiopental-induced decrease in GM1 ganglioside (GM1) levels in nerve growth factor-treated PC12 (PC12N) cells. PC12N cells were incubated for 24h in the presence or absence of (A) 20 µm propofol or (B) 100 µm thiopental after pretreatment with bicuculline at the indicated concentrations or without bicuculline pretreatment. Treated cell lysates were subjected to western blotting using horseradish peroxidase-conjugated cholera toxin B subunit (CTX–HRP). GM1 levels were determined by densitoscanning the blot after incubation with CTX–HRP, and band densities are presented as percentages of the control (vehicle-treated PC12N cells). Each column represents the mean of six values ± SD. *P < 0.0001 (one-way ANOVA combined with Scheffe test).

A γ aminobutyric acid A receptor inhibitor suppressed the propofol- or thiopental-induced decrease in GM1 ganglioside (GM1) levels in nerve growth factor-treated PC12 (PC12N) cells. PC12N cells were incubated for 24h in the presence or absence of (A) 20 µm propofol or (B) 100 µm thiopental after pretreatment with bicuculline at the indicated concentrations or without bicuculline pretreatment. Treated cell lysates were subjected to western blotting using horseradish peroxidase-conjugated cholera toxin B subunit (CTX–HRP). GM1 levels were determined by densitoscanning the blot after incubation with CTX–HRP, and band densities are presented as percentages of the control (vehicle-treated PC12N cells). Each column represents the mean of six values ± SD. *P < 0.0001 (one-way ANOVA combined with Scheffe test).

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