|Alternative Title||Neurnal mechanisms underlying the divergent effect of depression on pain|
Studies have reported divergent behavioral effects of depression on spontaneous vs. stimulus-evoked pain. However, the underlying neurobiological mechanisms are still unclear. The unpredictable chronic mild stress (UCMS) for rodent depression was employed in this experiment to investigate the internal relations between spontaneous pain and evoked pain, and to explore the mechanism of the divernt effect of depression on pain. Important findings were as following:
( 1 ) The results demonstrated that the processing of spontaneous vs. evoked pain in a depressive-like state was altered in the opposite direction (activation vs. inhibition). The ensemble encoding analysis revealed that exposure to UCMS gave rise to enhanced inter-regional functional connectivity in spontaneous pain processing, but did not influence that of evoked pain. In addition, different brain activation patterns underlying the processing of spontaneous vs. evoked pain were observed.
(2) The repeated high-frequency noxious radiant heat stimulus could induce the hyperalgesia phenomcnon9 and the system injection of 5-HT1A receptor antagonist could intensify the hyperalgesia phenomenon. In the rats with depressive-like behavior, behavioral study found that with the increased repeated number of high-frequency noxious radiant heat stimulus, the phenomenon of decreased sensitivity to radiant heat stimulus was disappeared.
(3) Pain-related conditioning training of depressive-like rats was employed in the present study. According this, we proved that the avoidance motive of rats with depression was significantly decreased, which maybe the important reason that depression could decrease the evoked pain.
In addition, I also demonstrated the collective contribution of medial and lateral pathway neurons to the noxious intensity coding. We provide evidence that ensemble spike count may be the most reliable method for coding pain intensity in the brain.
|Keyword||抑郁 疼痛 多通道神经元同步记录 自发痛 诱发痛|
|王宁. 抑郁对疼痛分离效应的神经机制研究[R]. 北京,2013.|
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