Journal
NEURON
Volume 91, Issue 4, Pages 851-862Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2016.07.016
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Funding
- NIH/NINDS
- Novo Nordisk
- European Union [666881]
- Rochester Institute of Technology
- Novo Nordisk Fonden [NNF13OC0004258] Funding Source: researchfish
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Energy production in the brain depends almost exclusively on oxidative metabolism. Neurons have small energy reserves and require a continuous supply of oxygen (O-2). 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 O-2-consuming neuropil, we have here examined whether activity-dependent dips in O-2 tension drive capillary hyperemia. In vivo analyses showed that transient dips in tissue O-2 tension elicit capillary hyperemia. Ex vivo experiments revealed that red blood cells (RBCs) themselves act as O-2 sensors that autonomously regulate their own deformability and thereby flow velocity through capillaries in response to physiological decreases in O-2 tension. This observation has broad implications for understanding how local changes in blood flow are coupled to synaptic transmission.
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