Boyeson M G, Harmon R L
Department of Rehabilitation Medicine, University of Wisconsin-Madison Medical School 53706.
Am J Phys Med Rehabil. 1993 Oct;72(5):286-93. doi: 10.1097/00002060-199310000-00007.
Rats pretrained to walk a narrow balance beam received unilateral sensorimotor cortex lesions, resulting in a contralateral transient paresis that lasted 14 days. In a dose-dependent manner, a single injection of the antidepressant trazodone given 24 hours after injury transiently slowed motor recovery compared with injured controls. After final recovery level of motor function, a reinjection of trazodone reinstated the hemiparesis for up to 6 hours. In other animals, a single injection of the antidepressant desipramine significantly facilitated motor performance when compared with injured controls. Desipramine had no deleterious motor effect when administered to animals that had recovered on the beam-walking task. These findings would suggest that the predominantly noradrenergic neurotransmitter effects of desipramine may facilitate, and those of the predominantly serotonergic trazodone may hinder, the recovery of locomotor performance after cortical injury in rats. Further studies appear indicated, including applying these findings to the clinical setting.
预先训练在狭窄平衡木上行走的大鼠接受了单侧感觉运动皮层损伤，导致对侧短暂性轻瘫，持续14天。与损伤对照组相比，在损伤后24小时单次注射抗抑郁药曲唑酮，以剂量依赖的方式短暂延缓了运动恢复。在运动功能达到最终恢复水平后，再次注射曲唑酮可使偏瘫恢复长达6小时。在其他动物中，与损伤对照组相比，单次注射抗抑郁药地昔帕明显著促进了运动表现。给在平衡木行走任务中已恢复的动物注射地昔帕明没有产生有害的运动影响。这些发现表明，地昔帕明主要的去甲肾上腺素能神经递质作用可能促进，而主要为血清素能的曲唑酮的作用可能阻碍大鼠皮质损伤后运动能力的恢复。似乎需要进一步的研究，包括将这些发现应用于临床环境。
