健康与遗传心理学研究室知识库

临床实践与基础研究表明，抑郁对诱发痛和自发痛的影响存在分离效应，即抑郁能够减弱诱发痛而增强自发痛，然而，这种分离效应的神经机制目前尚不清楚。本人在站期间的研究采用不确定预期的慢性温和应激模型作为抑郁动物模型，通过清醒动物电生理技术以及行为药理学等技术，探索抑郁对诱发痛和自发痛存在分离效应的成因，并试图阐明抑郁影响疼痛的神经机制。

主要发现如下:

( 1)通过对抑郁状态下所记录到的大鼠内外侧疼痛通路对诱发痛和自发痛的神经活动进行分析发现，给予大鼠自发痛时，抑郁组大鼠内侧和外侧通路的神经元活动都显著增加，而在给予大鼠诱发痛刺激时，抑郁组大鼠内外侧通路的神经活动减弱。

(2)高频多次的热辐射诱发痛能够产生痛觉过敏现象，且5-轻色胺能受体拮抗剂能够增强这种痛敏现象，当热辐射诱发痛刺激的次数较少时，抑郁能够减弱诱发痛，但是随着诱发痛次数的增加，这种减弱效应将会消失。

(3)抑郁情绪造成的伤害性回避动机减弱可能是前期研究中抑郁减弱诱发痛的重要因素。

此外，本人在站期间探索了内外侧疼痛通路对激光诱发痛的神经编码，证实了疼痛内侧通路与外侧通路具有类似的编码疼痛强度的能力，且神经元群体的编码对于强度编码来说更为有效。

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.