Nitric oxide and the cerebral-blood-flow response to somatosensory activation following deafferentation

The single-vibrissa stimulation model in the rat was utilized to study the microvascular coupling between functional activation and local cerebral blo od flow (LCBF) in both normal cortex and in cortex that had been peripheral ly deafferented. In addition, the role of chronic nitric oxide synthase (NO S) inhibition on the LCBF response to vibrissa stimulation was examined. On e-day-old rats underwent deafferentation of all vibrissae on one side of th e face, sparing C3, and received daily administration of either saline or N W-nitro-L-arginine (L-NA). After seven weeks of treatment, LCBF was measure d autoradiographically in conscious rats with [C-14]N-isopropyl-p-iodoamphe tamine while C3 was stimulated bilaterally Stimulation produced a greater i ncrease in LCBF in the deafferented cortex of both the saline (30.4%) and L -NA treated (25.7%) animals than in the intact cortex (19.9% and 16%, respe ctively). The area of activation of LCBF (0.176 mm(2)) was comparable to th e area metabolically activated (0.149 mm(2)), and the increase in area of L CBF activation following deafferentation (169%) was smaller than the increa se in area that was metabolically activated (287%). Chronic inhibition of N OS did not alter the spatial extent of the blood-flow response.