Abstract
Cerebral blood flow is vital for the survival and function of the brain. In particular, the hippocampus and cerebral cortex are very sensitive to transient ischemia. The hippocampus and cerebral cortex receive cholinergic vasodilative fibers that originate in the medial septum and the nucleus basalis of Meynert (NBM), respectively, of the basal forebrain (see a review by Sato et al., 1995, Alzheimer Dis. Assoc. Disord. 9: 28). Recently, we showed that increases in blood flow in the hippocampus and cerebral cortex in rats during activation of the vasodilative system, either by pharmacological (i.v. nicotine) or physiological (electrical stimulation of the NBM) methods, can prevent delayed death of hippocampal and cortical neurons following transient ischemia. Stimulation of the NBM increased the diameter of cortical parenchymal microvessels during stimulation. In addition, after the end of stimulation, an increase in the concentration of brain-derived neurotrophic factor (BDNF) in the cortical extracellular fluid was observed. From these findings, we suggest that activation of the intracranial vasodilative system provides protection against ischemia-induced delayed neuronal death by inducing increases in both the diameter of parenchymal microvessels and the release of an endogenous neuroprotective factor, BDNF. We also showed that activation of the vasodilative system occurred during passive somatosensory stimuli and active movements such as walking. Thus, this intracranial vasodilative system may contribute to the beneficial effect of physical activity on cognitive brain functions. [J Physiol Sci. 2006;56 Suppl:S26]
