Abstract

We examined whether streptozotocin-induced diabetes can modulate β-endorphin-induced antinociception in mice. While β-endorphin administered i.c.v. produced a dose-dependent inhibition of the tail-flick response in both diabetic and non-diabetic mice, the antinociceptive response was greater in diabetic mice than in non-diabetic mice. The ED 50 value of β-endorphin administered i.c.v. in diabetic mice was significantly lower than that in non-diabetic mice. The antinociceptive effects of β-endorphin administered i.c.v. in both diabetic and non-diabetic mice were significantly antagonized by s.c. administration of naltrindole, a selective δ-opioid receptor antagonist. β-Endorphin administered i.t. also produced a dose-dependent antinociception in both diabetic and non-diabetic mice. However, the ED 50 value of β-endorphin administered i.t. in diabetic mice was significantly higher than that in non-diabetic mice. The antinociceptive effect of β-endorphin administered i.t. in both diabetic and non-diabetic mice were significantly antagonized by s.c. administration of nor-binaltorphimine, a selective κ-opioid receptor antagonist. On the other hand, the antinociceptive potency of DPDPE, a selective δ-opioid agonist, administered i.t. is significantly increased in diabetic mice, as compared with non-diabetic mice, whereas, the antinociceptive potency of U-50,488H, a κ-opioid receptor agonist, administered i.t. is significantly less than in non-diabetic mice. These results suggest that diabetes may modulate β-endorphin-induced antinociception differently at the spinal and supraspinal levels.

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