The decreased endomorphin 2 and μ receptor in spinal cord of the STZ-induced type 1 diabetic rats is associated with painful diabetic neuropathy
作者单位：Department of Anatomy and K.K.Leung Brain Research Centre The Fourth Military Medical University Collaborative Innovation Center for Brain Science Fudan University
会议名称：《中国神经科学学会第十二届全国学术会议》
会议日期：2017年
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 100204[医学-神经病学] 10[医学]
摘 要：Painful diabetic neuropathy（PDN） is one of the most common complications at the early stage of diabetes mellitus（DM）. Both diabetic patients and animals frequently exhibit increased responsiveness to nociceptive stimuli. Endomorphin 2（EM2） has been implicated in selectively activating m opioid receptor（MOR） and subsequent induce antinociceptive effects in spinal dorsal horn. However, the mechanisms of EM2 and MOR in PDN have yet to be clarified in spinal dorsal horn. Therefore, we aimed to explore the role of EM2-MOR to determine the mechanism involved in the pathogenesis of PDN. The main findings were:（1） STZ-induced diabetic rats exhibited hyperglycemia, body weight loss and mechanical allodynia.（2） In spinal dorsal horn, the expressions of EM2 and MOR decreased in diabetic rats.（3） EM2 protein concentrations decreased in brain, lumbar spinal cord and CSF in diabetic rats, but were unchanged in plasma.（4） The frequency but not amplitude of spontaneous EPSCs（sEPSCs） was significantly higher in diabetic than control rats.（5） Intrathecal injection of EM2 for 14 days from the early stage of DPN alleviate mechanical allodynia and partially attenuated reduced MOR expression via Ser375 phosphorylation in diabetic rats. In summary, our results demonstrate that the impairment of endogenous analgesia system mediated by EM2 via MOR might be involved at the early stage of PDN.