Institoris Ádám, Rosenegger David George, Gordon Grant Robert
Hotchkiss Brain Institute, Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Department of Physiology, Faculty of Medicine, University of Szeged, Szeged, Hungary.
J Cereb Blood Flow Metab. 2015 Sep;35(9):1411-5. doi: 10.1038/jcbfm.2015.141. Epub 2015 Jul 1.
Ca(2+)-dependent pathways in neurons and astrocyte endfeet initiate changes in arteriole diameter to regulate local brain blood flow. Whether there exists a threshold of synaptic activity in which arteriole diameter is controlled independent of astrocyte endfeet Ca(2+) remains unclear. We used two-photon fluorescence microscopy to examine synaptically evoked synthetic or genetic Ca(2+) indicator signals around penetrating arterioles in acute slices of the rat neocortex. We discovered a threshold below which vasodilation occurred in the absence of endfeet Ca(2+) signals but with consistent neuronal Ca(2+) transients, suggesting endfoot Ca(2+) is not necessary for activity-dependent vasodilation under subtle degrees of brain activation.
神经元和星形胶质细胞终足中依赖钙的信号通路引发小动脉直径变化,以调节局部脑血流。目前尚不清楚是否存在一个突触活动阈值,在此阈值下小动脉直径的控制独立于星形胶质细胞终足钙信号。我们使用双光子荧光显微镜检查大鼠新皮质急性切片中穿透小动脉周围由突触诱发的合成或基因钙指示剂信号。我们发现了一个阈值,低于该阈值时,在没有终足钙信号但神经元钙瞬变一致的情况下会发生血管舒张,这表明在轻微程度的脑激活下,终足钙对于活动依赖性血管舒张并非必需。