Lesions of the basal forebrain in rat selectively impair the cortical vasodilation elicited from cerebellar fastigial nucleus.

We sought to determine in rat, whether interruption of the major extrathalamic projections to the cerebral cortex originating in and projecting through the basal forebrain (BF), will impair the increase in regional cerebral blood flow (rCBF), but not metabolism, elicited in the cerebral cortex by electrical stimulation of the cerebellar fastigial nucleus (FN). Studies were conducted in anesthetized, paralyzed, ventilated rats, with blood gases controlled and AP maintained in the autoregulated range. Electrolytic lesions were placed unilaterally in the BF at the level of the lateral preoptic region lying in rostral portions of the medial forebrain bundle and resulted in a reduction of up to 47% of the choline acetyltransferase activity in the ipsilateral cerebral cortex. rCBF was measured in homogenates of 9 paired brain regions by the 14C-iodoantipyrine technique. In unlesioned rats, FN stimulation symmetrically and significantly (P less than 0.05) increased rCBF in all brain regions with the greatest increase (to 180%) in the frontal cortex. Two days following a unilateral BF lesion, FN stimulation failed to increase rCBF in the ipsilateral cerebral cortex distal to the BF lesion. In contrast, rCBF was increased to an almost comparable degree in the remainder of the brain. BF lesions alone resulted in a 18-23% reduction in cortical rCBF ipsilaterally (P less than 0.025). BF lesions did not alter the cerebrovascular vasodilation elicited by CO2 nor perturb autoregulation. The cortical vasodilation elicited by FN stimulation is mediated by intrinsic neuronal pathways and depends upon the integrity of neurons, possibly cholinergic, originating in, or passing through, the BF.