EFFECTS OF ACTIVATING THE CHOLINERGIC VASODILATIVE SYSTEM ORIGINATING IN THE BASAL FOREBRAIN ON BLOOD FLOW AND DELAYED NEURONAL DEATH FOLLOWING TRANSIENT ISCHEMIA

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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) and septal complex in the basal forebrain and projecting to the cortex and hippocampus was recently demonstrated. In the present study, we aimed to clarify whether the increase in CBF following stimulation of the NBM or septal complex can improve delayed death of the cortical or hippocampal neurons following transient ischemia in rats.Cortical and hippocampal CBF was measured using a laser Doppler flowmeter, and delayed neuronal death of the cerebral cortex or hippocampus produced by intermittent (every 5 s) occlusions of the unilateral common carotid artery for 60 min was measured histologically in the cortical hemisphere. In the case of study on hippocampus, permanent ligation of bilateral vertebral arteries was previously performed.The increase in cortical CBF induced by NBM stimulation prevented the occlusion-induced decrease in cortical CBF, and the delayed death of the cortical neurons previously observed after the occlusions was scarcely observable. The increase in hippocampal CBF induced by stimulating the medial septum prevented the occlusion-induced decrease in hippocampal CBF, and the delayed death of the hippocampal CA1 neurons previously observed after the occlusions was scarcely observable.The present results suggest that basal forebrain-originating vasodilative activation can protect ischemia-induced delayed death of cortical and hippocampal neurons by preventing a blood flow decrease in cortex and hippocampus.