Modifications of supraspinal pain pathway by diabetes in mice

感觉异常是糖尿病的严重并发症，给患者的生活带来诸多不便。目前尚无针对此并发症的治疗方案。本研究通过实验性糖尿病小鼠模型，探讨糖尿病感觉异常的新机制。丘脑内谷氨酸NMDA和AMPA受体拮抗剂治疗降低糖尿病小鼠的热和机械超敏反应。这种处理不影响非糖尿病小鼠的热和机械阈值。用谷氨酸、NMDA受体激动剂和AMPA受体激动剂对小鼠进行丘脑内处理，产生机械和热超敏反应。此外，糖尿病小鼠丘脑小胶质细胞标记物Iba1的表达增加。这些结果表明，糖尿病患者的异常感觉知觉可能部分是由于疼痛通路在脊柱上部位的敏感化。

Abnormal sensory perception in diabetes mellitus is very severe complications, which make patent life very inconvenient. The curative regimen for this complication does not established so far. The present study was investigate the novel mechanisms underlying in the diabetic sensory abnormal perception in the experimentally (streptozotocin-treated) induced diabetic mouse model. Intra-thalamic treatment with glutamate NMDA and AMPA receptor antagonist reduced the thermal and mechanical hypersensitivity in diabetic mice. This treatment did not affect the thermal and mechanical threshold in non-diabetic mice. Intra-thalamic treatment with glutamate, NMDA receptor agnonist and AMPA receptor agonist produced mechanical and thermal hypersensitivity in mice. Moreover, the expression of microglial marker Iba1 immunoreactivity was increased in diabetic mouse thalamus. These results suggested that abnormal sensory perception in diabetes mellitus may be due, in part, to the sensitization of pain pathway in the supraspianal site.