Neurovascular coupling during hypercapnia in cerebral blood flow regulation

Abstract

Neuronal activity consumes cellular energy and generates carbon dioxide (CO2). To counter this metabolic challenge, synaptic signalling communicates with nearby microvasculature to increase local blood flow. Is this process solely based on feedforward synaptic signalling, or is the generated CO2 also involved? This question was addressed in mice in a new Nature Communications publication by Tournissac and colleagues where they showed that neurovascular coupling is not affected by exogenous CO2 or its associated acidification.