Fig. 3. Increased sensitivity to isoflurane-induced antinociception in the GluR2 null mutant (−/−) mice. Hind-paw withdrawal latency (HPWL) times measured in concentrations of isoflurane (0.1, 0.2, 0.4, and 0.6 MAC) were normalized to baseline values and averaged (mean ± SD) for wild-type (+/+) mice (closed squares) and (−/−) mice (open triangles). In (−/−) mice, HPWL increased dose-dependently with higher concentrations of isoflurane administered. HPWL increased 36, 42, 68, and 140% above baseline with 0.1, 0.2, 0.4, and 0.6 MAC of isoflurane, respectively (* P < 0.01). In contrast, (+/+) mice showed lesser increases in HPWL with 0.1, 0.2, 0.4, and 0.6 MAC of isoflurane (8, 3, 19, and 65%, respectively). The HPWL at 0.2, 0.4, and 0.6 MAC of isoflurane in the (−/−) mice were significantly prolonged compared with values obtained for (+/+) mice (** P < 0.05).

Fig. 3. Increased sensitivity to isoflurane-induced antinociception in the GluR2 null mutant (−/−) mice. Hind-paw withdrawal latency (HPWL) times measured in concentrations of isoflurane (0.1, 0.2, 0.4, and 0.6 MAC) were normalized to baseline values and averaged (mean ± SD) for wild-type (+/+) mice (closed squares) and (−/−) mice (open triangles). In (−/−) mice, HPWL increased dose-dependently with higher concentrations of isoflurane administered. HPWL increased 36, 42, 68, and 140% above baseline with 0.1, 0.2, 0.4, and 0.6 MAC of isoflurane, respectively (* P < 0.01). In contrast, (+/+) mice showed lesser increases in HPWL with 0.1, 0.2, 0.4, and 0.6 MAC of isoflurane (8, 3, 19, and 65%, respectively). The HPWL at 0.2, 0.4, and 0.6 MAC of isoflurane in the (−/−) mice were significantly prolonged compared with values obtained for (+/+) mice (** P < 0.05).

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