Both clinical and laboratory studies had shown that depression reduced evoked pain and increased spontaneous pain. This phenomenon was proved to be associated with neuron activity in the medial/ lateral (affective/sensory) pain pathways. However, studies on depression differential regulation of evoked and spontaneous pain have not been integrated in the same individual, with little attention to the dorsal horn of the spinal cord until now. The project bases on our previous work, intends to use behavioral, immunohistochemistry, neuropharmacology and molecular biology methods and employs L5 SNL which exhibits both allodynia and spontaneous pain as a neuropathic pain model. We are taking the expression of glucocorticoid receptor as a breakthrough point, trying to examine if depression could reduce tactile allodynia, and explore the neural mechanism of sensory regulation in spinal dorsal horn under this situation. At the same time, we employ conditioned place preference paradigm to examine if depression could increase spontaneous pain, and explore the neural mechanisms of affective pain regulation in anterior cingulate cortex. In this study, the impact of depression on pain was observed and explained comprehensively on both sensory and affective aspects. It is not only a powerful complement for the mechanism of depression on pain, but also providing important evidences and inspiration for the clinical treatment of depression and pain comorbidity, which exhibits innovative features and extensive potential of application.
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