2002 Volume 52 Issue 4 Pages 383-393
An increase in cortical cerebral blood flow (CBF), independent of metabolic vasodilation, via the activation of cholinergic neurons originating in the nucleus basalis of Meynert (NBM) in the basal forebrain and projecting to the widespread cortices was recently demonstrated. In the present study, we aimed to clarify whether the increase in CBF following a stimulation of the NBM can improve delayed death of the cortical neurons following transient ischemia in rats. CBF was measured with a laser Doppler flowmeter, and the delayed neuronal death of the cerebral cortex produced by intermittent (every 5 s) occlusions of the unilateral common carotid artery for 60 min was measured histologically in the cortical hemisphere at 3 different coronal levels (6 μm thickness). In control rats without occlusion there were 6,000–8,000 intact neurons and 9–19 damaged neurons in the cortical hemisphere at each coronal level. During the occlusions, CBF ipsilateral to the occluded artery decreased by 13–32% of the preocclusion level. Five days after the occlusions, the numbers of damaged neurons were increased to 75–181. Repetitive electrical stimulation was delivered to the NBM, ipsilateral to the occluded artery, starting 5 min before the occlusions and finishing around the end of them. The increase in CBF induced by NBM stimulation prevented the occlusion-induced decrease in CBF in all 3 of the cortices. The delayed death of the cortical neurons previously observed after the occlusions was scarcely observable in all the cortices when NBM was stimulated. The present results suggest that NBM-originating vasodilative activation can protect the ischemia-induced delayed death of cortical neurons by preventing a blood flow decrease in widespread cortices.
