Wei Helen Shinru, Kang Hongyi, Rasheed Izad-Yar Daniel, Zhou Sitong, Lou Nanhong, Gershteyn Anna, McConnell Evan Daniel, Wang Yixuan, Richardson Kristopher Emil, Palmer Andre Francis, Xu Chris, Wan Jiandi, Nedergaard Maiken
Center for Translational Neuromedicine, University of Rochester Medical Center, Rochester, NY 14642, USA.
Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Neuron. 2016 Aug 17;91(4):851-862. doi: 10.1016/j.neuron.2016.07.016. Epub 2016 Aug 4.
Energy production in the brain depends almost exclusively on oxidative metabolism. Neurons have small energy reserves and require a continuous supply of oxygen (O2). It is therefore not surprising that one of the hallmarks of normal brain function is the tight coupling between cerebral blood flow and neuronal activity. Since capillaries are embedded in the O2-consuming neuropil, we have here examined whether activity-dependent dips in O2 tension drive capillary hyperemia. In vivo analyses showed that transient dips in tissue O2 tension elicit capillary hyperemia. Ex vivo experiments revealed that red blood cells (RBCs) themselves act as O2 sensors that autonomously regulate their own deformability and thereby flow velocity through capillaries in response to physiological decreases in O2 tension. This observation has broad implications for understanding how local changes in blood flow are coupled to synaptic transmission.
大脑中的能量产生几乎完全依赖于氧化代谢。神经元的能量储备较少,需要持续的氧气(O2)供应。因此,正常脑功能的一个标志是脑血流量与神经元活动之间的紧密耦合也就不足为奇了。由于毛细血管嵌入消耗氧气的神经纤维中,我们在此研究了氧气张力的活动依赖性下降是否会驱动毛细血管充血。体内分析表明,组织氧气张力的短暂下降会引发毛细血管充血。体外实验表明,红细胞(RBCs)本身充当氧气传感器,可自主调节自身的变形能力,从而响应氧气张力的生理下降来调节通过毛细血管的流速。这一观察结果对于理解血流的局部变化如何与突触传递相耦合具有广泛的意义。