神经病理性疼痛常诱发抑郁样情绪，导致患者遭受痛觉体验远超越疼痛固有的生

Neuropathic pain often induced depression-like mood, resulting in patients suffering from pain experience far beyond the inherent biological effects of pain, central nervous system signaling pathway involved in epigenetic modifications induced depression-like behaviors role in chronic pain are more and more concerns specific regulatory mechanisms are not yet clear. We previously found before depression-like behaviors in mice induced neuropathic pain and cingulate cortex circ_0000416 lacuna protein -1 (caveolin-1) NMDA channel signal molecule expression / upregulated, miRNA-107 is circ_0000416 target gene, but the mechanism involves the corresponding pathological process has not been reported. The project intends to use behavior, bioinformatics, electrophysiological and molecular biology techniques to explore further the relationship between circ_0000416 interaction and miRNA-017, and further elucidate the mechanism of its signal pathway mediated upregulation of expression of caveolin-1 in the regulation of activation neuropathic pain induced depression-like behaviors and molecular mechanisms of action, provide new targets and experimental basis for the prevention and treatment of disease.

Neuropathic pain often induces depression-like emotions, leading to patients suffering from pain experience far beyond the inherent biological effects of pain, the central nervous system epigenetic modification involved in the role of signaling pathway regulation in chronic pain-induced depression-like behavior has received more and more attention, the specific regulatory mechanism has not been clear. We found earlier that neuropathic pain induced depression-like behavior in mice with pre-buckles to bring back cortical circ_0000416 and trap protein-1 (caveolin-1)/NMDA pathway signal molecular expression significantly increased, miRNA-107 is the target gene of circ_0000416, but its mechanism involving the corresponding pathological processes has not been reported. This project intends to use behavioral, bioinformatics, electrophysiology and molecular biology to explore the interaction between circ_0000416 and miRNA-017, and then clarify the mechanism of caveolin-1 expression upward and its mediated signal path activation in regulating neuropathic pain-induced depressive-like behavior and molecular mechanisms, to provide new targets and experimental basis for disease prevention and treatment.

Neuropathic pain often induces depression like emotion, which leads to patients suffering from pain experience far beyond the intrinsic biological effect of pain. The role of signal pathway regulation involved in epigenetic modification of central nervous system in chronic pain induced depression like behavior has been more and more concerned, and the specific regulatory mechanism has not been clear. We previously found that the expression of circ_andcaveolin-1 / NMDA pathway signal molecules in the anterior cingulate cortex of depression like behavior mice induced by neuropathic pain was significantly up-regulated. Mirna-107 is the target gene of circ_, but the mechanism involved in the corresponding pathological process has not been reported. In this project, behavioral, bioinformatics, electrophysiology and molecular biology technologies are used to explore the interaction between circ_andmirna-017, so as to clarify the mechanism of up regulation of caveolin-1 expression and the role and molecular mechanism of its signal pathway activation in the regulation of depression like behavior induced by neuropathic pain, so as to provide new targets and experimental basis for disease prevention and treatment.