Suzuki T, Hayashi Y, Misawa M
Department of Applied Pharmacology, School of Pharmacy, Hoshi University, Japan.
Life Sci. 1992;50(12):849-56. doi: 10.1016/0024-3205(92)90203-2.
It is known that the CXBK inbred strain of mouse is deficient in mu1 opioid receptors, whereas the strain has a delta opioid receptor population that is less consistently altered. In the present study, we compared physical dependence on morphine between CXBK and C57BL/6 mice. Both strains of mice were treated with morphine-admixed food for 5 days. During the treatment, the two strains of mice showed no signs of toxicity. There was no significant difference in morphine intake during the treatment between CXBK and C57BL/6 mice. After the treatment, the withdrawal was precipitated by injecting naloxone (0.01-30 mg/kg, s.c.). CXBK mice showed weight loss, diarrhea and ptosis, but not jumping and body shakes after low dose of naloxone. Whereas, C57BL/6 mice showed weight loss, diarrhea, ptosis, body shakes and jumping. These results suggest that naloxone-precipitated weight loss, diarrhea and ptosis may be mediated by mu2 and/or delta opioid receptor, while naloxone-precipitated jumping and body shakes may be mediated by mu1 opioid receptors.
已知CXBK近交系小鼠缺乏μ1阿片受体，而该品系的δ阿片受体群体变化不太一致。在本研究中，我们比较了CXBK小鼠和C57BL/6小鼠对吗啡的身体依赖性。两种品系的小鼠均用含吗啡的食物处理5天。处理期间，两种品系的小鼠均未出现中毒迹象。CXBK小鼠和C57BL/6小鼠在处理期间的吗啡摄入量无显著差异。处理后，通过皮下注射纳洛酮（0.01 - 30 mg/kg）引发戒断反应。低剂量纳洛酮处理后，CXBK小鼠出现体重减轻、腹泻和眼睑下垂，但未出现跳跃和身体颤抖。而C57BL/6小鼠出现体重减轻、腹泻、眼睑下垂、身体颤抖和跳跃。这些结果表明，纳洛酮引发的体重减轻、腹泻和眼睑下垂可能由μ2和/或δ阿片受体介导，而纳洛酮引发的跳跃和身体颤抖可能由μ1阿片受体介导。
