Erythrocytes Are Oxygen-Sensing Regulators of the Cerebral Microcirculation
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Erythrocytes Are Oxygen-Sensing Regulators of the Cerebral Microcirculation. / 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.
In: Neuron, Vol. 91, No. 4, 17.08.2016, p. 851-862.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Erythrocytes Are Oxygen-Sensing Regulators of the Cerebral Microcirculation
AU - Wei, Helen Shinru
AU - Kang, Hongyi
AU - Rasheed, Izad-Yar Daniel
AU - Zhou, Sitong
AU - Lou, Nanhong
AU - Gershteyn, Anna
AU - McConnell, Evan Daniel
AU - Wang, Yixuan
AU - Richardson, Kristopher Emil
AU - Palmer, Andre Francis
AU - Xu, Chris
AU - Wan, Jiandi
AU - Nedergaard, Maiken
N1 - Copyright © 2016 Elsevier Inc. All rights reserved.
PY - 2016/8/17
Y1 - 2016/8/17
N2 - 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.
AB - 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.
KW - Journal Article
U2 - 10.1016/j.neuron.2016.07.016
DO - 10.1016/j.neuron.2016.07.016
M3 - Journal article
C2 - 27499087
VL - 91
SP - 851
EP - 862
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 4
ER -
ID: 164971619