Abstract
The role of the noradrenergic (NE) system in recovery of motor function after sensorimotor cortex (SMCX) injury was investigated. After training on a beam-walking task to assess changes in motor function, animals were given DSP-4 or saline and tested for 2 weeks; both groups then received unilateral SMCX suction ablations. Animals that received DSP-4 were significantly retarded in motor recovery compared with the saline group. At 24 days after injury (after motor recovery), the animals' deficits were significantly reinstated with NE-blocking drugs. DSP-4 significantly depressed NE levels in the hippocampus and cerebellum. A Timm histochemical analysis revealed glutamatergic sprouting in the hippocampus of animals that were pretreated with DSP-4, which suggests the possibility that similar glutamatergic plasticity in other pathways may occur and that excitotoxicity might also play a role after the DSP-4 induced NE deafferentation.
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