Modifications of supraspinal pain pathway by diabetes in mice

糖尿病患者的感觉异常是非常严重的并发症，给患者的生活带来不便。迄今为止，这种并发症的治疗方案尚未确定。本研究旨在探讨链脲佐菌素诱导的糖尿病小鼠模型中糖尿病感觉异常的新机制。谷氨酸NMDA和AMPA受体拮抗剂在丘脑内治疗可降低糖尿病小鼠的热和机械超敏反应。该处理对非糖尿病小鼠的热、力学阈值无影响。谷氨酸、NMDA受体激动剂和AMPA受体激动剂在丘脑内治疗小鼠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志物Iba1免疫反应性表达增加。这些结果提示，糖尿病的感觉异常可能部分是由于腹膜上部位疼痛通路的敏化所致。

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.