Fig. 3. Pooled summary data of study 1. (Top ) Mean values ± SD of normalized peak neuronal discharge frequency (Fn; %) before (Fcon) and during (Fe) maximal GABAAergic block with bicuculline (BIC) for the 0 minimum alveolar concentration (MAC), 1 MAC, and 0 MAC end-control doses for 14 neurons. At all MAC levels, Fewas significantly greater than Fcon(***P < 0.001). Halothane, 1 MAC, caused a significant reduction of Fcon(§§§P < 0.001) and Fe(###P < 0.001). The 0-MAC end-control values for Fconwere not different (not significant) from the initial 0 MAC values, indicating stability of the preparation. A small but significant decline in Fe(7.4 ± 16.7%) of the end control was present (#P < 0.05). (Bottom ) Mean depression ± SD of overall excitatory drive, (ΔFe), mean enhancement of inhibitory neurotransmission (Δα), and the resulting mean depression of control frequency (ΔFcon) by 1 MAC halothane in 14 neurons. (†P < 0.05, ††P < 0.01, †††P < 0.001 relative to no change.)

Fig. 3. Pooled summary data of study 1. (Top ) Mean values ± SD of normalized peak neuronal discharge frequency (Fn; %) before (Fcon) and during (Fe) maximal GABAAergic block with bicuculline (BIC) for the 0 minimum alveolar concentration (MAC), 1 MAC, and 0 MAC end-control doses for 14 neurons. At all MAC levels, Fewas significantly greater than Fcon(***P < 0.001). Halothane, 1 MAC, caused a significant reduction of Fcon(§§§P < 0.001) and Fe(###P < 0.001). The 0-MAC end-control values for Fconwere not different (not significant) from the initial 0 MAC values, indicating stability of the preparation. A small but significant decline in Fe(7.4 ± 16.7%) of the end control was present (#P < 0.05). (Bottom ) Mean depression ± SD of overall excitatory drive, (ΔFe), mean enhancement of inhibitory neurotransmission (Δα), and the resulting mean depression of control frequency (ΔFcon) by 1 MAC halothane in 14 neurons. (†P < 0.05, ††P < 0.01, †††P < 0.001 relative to no change.)

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