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Changes in Analgesia-Producing Mechanism of Repeated Cold Stress Loading in Mice

2000; Elsevier BV; Volume: 65; Issue: 2 Linguagem: Inglês

10.1016/s0091-3057(99)00215-4

1873-5177

Yuji Omiya, Kazuhiro Goto, Atsushi Ishige, Yasuhiro Komatsu,

Stress Responses and Cortisol

Functional changes in opioid receptors involved in analgesia of repeated cold stress (RCS)-loaded mice were investigated. The antinociceptive potency of morphine (4 mg/kg, PO) was not affected in normal mice by norbinaltorphimine (10 mg/kg, SC), but treatment with this agent resulted in a lower level of morphine-induced antinociception in RCS-loaded animals. The antinociceptive activity of U-50488H (3 mg/kg, SC) was increased in RCS-loaded mice. In contrast to hypersensitivity to U-50488H (1 and 10 μg, IT) noted in RCS-loaded mice, the antinociception induced by DAMGO (0.1 and 1 μg, ICV) was reduced compared to that of normal animals. Diazepam (1 mg/kg/day SC) was given during RCS loading, and this agent prevented the development of hyperalgesia and the decrease in the antinociceptive activity of DAMGO (1 μg, ICV) in RCS-loaded mice, but there was no effect on the enhancement of the antinociceptive potency of U-50488H (10 μg, IT). These results indicate that the RCS-loaded mice were hyposensitive to supraspinal μ-opioid receptor-mediated antinociception, whereas their antinociceptive activities through κ-opioid receptor in the spinal cord were increased. Hypofunction of the supraspinal μ-opioid receptor due to anxiety may explain the mechanism involved in the lowering of the nociceptive threshold in RCS-loaded animals.