Krupina N A, Orlova I N, Khlebnikova N N, Grafova V N, Smirnova V S, Kukushkin M L, Kryzhanovskii G N, Pankova N B, Rodina V I
Laboratory of General Pathophysiology of Nervous System, Moscow.
Bull Exp Biol Med. 2002 Jun;133(6):548-52. doi: 10.1023/a:1020217421991.
Modeling of neurogenic pain syndrome by sciatic nerve transection in rats with pronounced dopamine-deficiency-dependent 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced experimental depressive syndrome forms a stable state of combined pain and depression, which can be considered as a model of the pain-depressive syndrome. The neurogenic pain syndrome prolongs the state of behavioral depression in rats irrespective of their initial anxiety level. The depressive symptoms can potentiate the severity of pain syndrome. By a number of indices, more pronounced behavioral changes during the development of pain-depressive syndrome occur in initially nonanxious rats.
在具有明显多巴胺缺乏依赖性1-甲基-4-苯基-1,2,3,6-四氢吡啶诱导的实验性抑郁综合征的大鼠中，通过坐骨神经横断术对神经源性疼痛综合征进行建模，形成了疼痛与抑郁合并的稳定状态，这可被视为疼痛-抑郁综合征的模型。无论大鼠最初的焦虑水平如何，神经源性疼痛综合征都会延长其行为抑郁状态。抑郁症状会加重疼痛综合征的严重程度。从一些指标来看，最初无焦虑的大鼠在疼痛-抑郁综合征发展过程中出现的行为变化更为明显。
