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

激活源自基底前脑的胆碱能血管舒张系统对短暂性缺血后血流和延迟性神经元死亡的影响

基本信息

批准号：
13670078
负责人：
HOTTA Harumi
金额：
$ 1.79万
依托单位：
Tokyo Metropolitan Institute of Gerontology
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2003
项目状态：
已结题

项目摘要

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.

与代谢血管舒张无关的皮质脑血流动（CBF）通过激活造成基底前头Meynert（NBM）核（NBM）核的胆碱能神经元的激活而增加，并在基础前脑中并投射到皮质和海马群中。 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 （每5 s）在皮质半球中测量组织学测量单侧共同颈动脉60分钟。在有关海马研究的研究中，先前进行了双侧椎动脉的永久连接。由NBM刺激引起的皮质CBF的增加阻止了闭塞性CBF的闭塞性CBF的降低，并且在闭塞后先前观察到的皮质神经元延迟死亡的延迟死亡。通过刺激内侧隔膜引起的海马CBF的增加阻止了闭塞引起的海马CBF的减少，以及先前观察到的闭塞后的海马CA1神经元延迟死亡的延迟死亡。海马神经元通过防止血液流量减少皮层和海马。