Summary
The mechanisms of neurovascular coupling remain incompletely understood. Here we show in experimental animal models that the neuronal activity-dependent increases in local cerebral blood flow in the somatosensory cortex are abolished by saturation of brain CO2-sensitive vasodilatory mechanism or disruption of brain HCO3-/CO2 transport, independently of baseline cerebral perfusion and brain tissue pH. These results suggest that increases in metabolic CO2 production and CO2 signalling play an important role in the development of neurovascular coupling response.
Competing Interest Statement
The authors have declared no competing interest.
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