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. 2002 Sep 15;22(18):8312–8323. doi: 10.1523/JNEUROSCI.22-18-08312.2002

Fig. 9.

Fig. 9.

Inhibition by MK-801 of morphine tolerance and thermal hyperalgesia potentiated by PDC. A, The development of thermal hyperalgesia was potentiated in rats treated with 10 μg of morphine plus 20 μg of PDC (B10+P20) but prevented in rats receiving 10 μg of morphine plus 20 μg of riluzole (B10+R20). PDC or riluzole alone changed baseline paw-withdrawal latencies (PWL) on day 8 but did not reach the statistical significance at the current dose.B, The morphine antinociception was dose-dependently reduced on day 8 in rats receiving 7 d intrathecal 20 μg of morphine boluses (B20). The GT activator riluzole (20 μg), given intrathecally at 30 min before the morphine antinociceptive test on day 8 (B20+R20; Day 8), did not reverse the behavioral manifestation of morphine tolerance. C, The development of morphine tolerance was potentiated by intrathecal coadministration of 10 μg of morphine with 20 μg of PDC (B10+P) twice daily for 7 d. This potentiation was blocked by adding 10 nm MK-801 into this combination (B+P+M). Treatment with 10 nm MK-801 alone (MK) for 7 d did not change the antinociceptive effects of morphine. *p < 0.05, **p < 0.01, as compared with the corresponding saline group, and+ p < 0.05,++ p < 0.01, as compared with the corresponding morphine alone group.