Fig. 5. Prostaglandin E2(PGE2)-evoked glutamate release using spinal cord slices from sham-operated and nerve-injured rats. The addition of PGE2produced concentration-dependent glutamate release from spinal cord slices of sham-operated (nonallodynic) animals (see table 1for EC50and 95% CI of each group). This effect was significantly enhanced (leftward shift) in slices from ligated (allodynic) rats. The concentration-response curve using slices from ligated rats treated with S(+)-ibuprofen (four intrathecal doses of 100 μg every 2 h, beginning 2 h after ligation), which prevented allodynia (fig. 3), was not significantly different from the sham-operated group. In contrast, slices from ligated rats treated with R(−)-ibuprofen, which had no effect on allodynia (fig. 3), yielded a concentration-response curve that was not significantly different from ligated, untreated (allodynic) rats. Each point  represents the mean ± SEM of at least five animals (5–14 slices).

Fig. 5. Prostaglandin E2(PGE2)-evoked glutamate release using spinal cord slices from sham-operated and nerve-injured rats. The addition of PGE2produced concentration-dependent glutamate release from spinal cord slices of sham-operated (nonallodynic) animals (see table 1for EC50and 95% CI of each group). This effect was significantly enhanced (leftward shift) in slices from ligated (allodynic) rats. The concentration-response curve using slices from ligated rats treated with S(+)-ibuprofen (four intrathecal doses of 100 μg every 2 h, beginning 2 h after ligation), which prevented allodynia (fig. 3), was not significantly different from the sham-operated group. In contrast, slices from ligated rats treated with R(−)-ibuprofen, which had no effect on allodynia (fig. 3), yielded a concentration-response curve that was not significantly different from ligated, untreated (allodynic) rats. Each point  represents the mean ± SEM of at least five animals (5–14 slices).

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