Abstract
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.
Keywords
Get full access to this article
View all access options for this article.