Department of Rehabilitation Medicine, University of Wisconsin Medical School, Madison, WI 53706 (USA).
Restor Neurol Neurosci. 1993 Jan 1;5(4):283-90. doi: 10.3233/RNN-1993-5404.
Previous research has indicated that antagonists of locus ceruleus functioning, when administered during the acute phase of an injury, slow recovery of motor function following unilateral sensorimotor cortex injury. Following a recovery plateau in animals, it is possible to pharmacologically reinstate unilateral motor deficits in recovered animals with similar acting drugs given intraperitoneally. The present study was designed to localize the brain systems responsible for the reinstatement of the deficit after recovery from the cortical injury. The results indicate that maintaining functional recovery after injury is modulated by NE in the cerebellum contralateral to the injury, since microinfusions of phenoxybenzamine into this structure reinstate motor deficits. Additionally, removal of the noradrenergic projection to contralateral cerebellum through unilateral lesions of the locus ceruleus reinstate unilateral deficits more severely than the drug administration.
先前的研究表明，在损伤的急性期给予蓝斑核功能拮抗剂，会减缓单侧感觉运动皮层损伤后运动功能的恢复。在动物进入恢复平台期后，用类似作用的药物经腹腔内给药，有可能使已恢复的动物的单侧运动缺陷重新出现。本研究旨在定位负责皮质损伤恢复后缺陷重新出现的脑系统。结果表明，小脑 NE 维持着损伤后的功能恢复，因为将苯氧苄胺微注入到该结构会使运动缺陷重新出现。此外，通过单侧损毁蓝斑核去除对侧小脑的去甲肾上腺素投射，会比药物给药更严重地重新出现单侧缺陷。
