Role of local neurons in cerebrocortical vasodilation elicited from cerebellum.

The vasodilation elicited in cerebral cortex by stimulation of the cerebellar fastigial nucleus (FN) is mediated by input pathways coming from the basal forebrain. We studied whether these pathways mediate the cortical vasodilation via a direct action on local blood vessels or via interposed local neurons. Neurons were destroyed in the primary sensory cortex by local microinjection of the excitotoxin ibotenic acid (IBO) (10 micrograms/l microliter). Five days later rats were anesthetized (alpha-chloralose), paralyzed, and ventilated. Arterial pressure and blood gases were controlled, and FN was stimulated electrically. Local cerebral blood flow (LCBF) was measured using the [14C]iodoantipyrine technique with autoradiography. Five days after IBO, neurons were destroyed in a restricted cortical area, and afferent fibers and terminals were preserved. The selectivity of the neuronal loss was established by histological and biochemical criteria and by transport of horseradish peroxidase from or into the lesion. Within the lesion, resting LCBF (n = 7) was unaffected, but the increase in LCBF evoked from the FN was abolished (P greater than 0.05); n = 6). In contrast the vasodilation elicited by hypercapnia (arterial CO2 partial pressure = 62.7 +/- 3; n = 5) was preserved. In the rest of the brain the vasodilation elicited from FN was largely unaffected. We conclude that the vasodilation evoked from FN in cerebral cortex depends on the integrity of a restricted population of local neurons that interact with the local microvasculature.