Pieper G M, Mizoguchi H, Ohsawa M, Kamei J, Nagase H, Tseng L F
Department of Surgery, Division of Transplant Surgery, Medical College of Wisconsin, Froedtert Memorial Lutheran Hospital, 9200 West Wisconsin Avenue, 53226, Milwaukee, WI, USA.
Eur J Pharmacol. 2000 Aug 11;401(3):375-9. doi: 10.1016/s0014-2999(00)00459-3.
Previous evaluation of antinociceptive action in experimental diabetes has been conducted almost exclusively in chemically induced diabetes mellitus. The purpose of the present study was to evaluate antinociceptive response and G-protein activation by mu-opioid receptor and delta-opioid receptor agonists in the genetic non-obese diabetic (NOD) mouse, a model of type I insulin-dependent diabetes mellitus (IDDM). Tail-flick latency before and after hyperglycemia was unaltered. Hyperglycemic NOD mice were hyporesponsive to intracerebroventricular (i.c.v.) injections of [D-Ala(2)]deltorphin II but not to [D-Ala(2), N-MePhe(4), Gly-ol(5)]enkephalin (DAMGO); however, G-protein activation in pons/medulla assessed by [35S]GTPgammaS binding was not diminished. This suggests that a G-protein defect in signaling cannot account for the hyporesponsiveness of antinociception in this genetic model of IDDM.
以往对实验性糖尿病中抗伤害感受作用的评估几乎完全是在化学诱导的糖尿病模型中进行的。本研究的目的是评估遗传性非肥胖糖尿病（NOD）小鼠（I型胰岛素依赖型糖尿病（IDDM）模型）中μ-阿片受体和δ-阿片受体激动剂的抗伤害感受反应和G蛋白激活情况。高血糖前后的甩尾潜伏期未改变。高血糖的NOD小鼠对脑室内（i.c.v.）注射[D-Ala(2)]deltorphin II反应低下，但对[D-Ala(2), N-MePhe(4), Gly-ol(5)]脑啡肽（DAMGO）无此反应；然而，通过[35S]GTPγS结合评估的脑桥/延髓中的G蛋白激活并未减弱。这表明在该IDDM遗传模型中，信号传导中的G蛋白缺陷不能解释抗伤害感受反应低下的现象。
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