FOCAL TRAUMATIC BRAIN INJURY CAUSES WIDESPREAD REDUCTIONS IN RAT-BRAIN NOREPINEPHRINE TURNOVER FROM 6 TO 24 H

The effect of right sensorimotor traumatic brain injury (TBI) in male Sprague-Dawley rats on brain norepinephrine (NE) turnover was assessed by measuring the decline of endogenous NE levels following tyrosine h ydroxylase inhibition produced with alpha-methyl-p-tyrosine. Right sen sorimotor cortex contusions were produced by a pneumatically driven pi ston which depressed the dural surface by 2 mm at 3.2 m/s. TBI rats we re compared to uninjured, anesthetized controls at 6 h and 24 h after surgery. While NE turnover was not affected at the lesion site at 6 h after TBI, it was either abolished or decreased by 33-75% bilaterally in the hypothalamus and in the cerebral cortex surrounding and rostral to the lesion site. In the cortex caudal to the lesion site, NE turno ver was completely abolished. NE turnover in cerebral cortex opposite the lesion site and in the contralateral cerebellum was decreased by 5 1 and 43%, respectively, at 6 h. At 24 h, NE turnover was either aboli shed or decreased bilaterally by 45-92% in all cortical areas, in the hypothalamus, cerebellum, locus coeruleus and medulla. Thus, right sen sorimotor cortex contusion causes a marked, early and widespread depre ssion of brain NE turnover. Since amphetamine increases NE turnover, t his may explain the dramatic improvement in behavioral deficits which occurs following amphetamine administration at 24 h after such lesions .