A. Dunnmeynell et al., FOCAL TRAUMATIC BRAIN INJURY CAUSES WIDESPREAD REDUCTIONS IN RAT-BRAIN NOREPINEPHRINE TURNOVER FROM 6 TO 24 H, Brain research, 660(1), 1994, pp. 88-95
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
.