Neurovascular coupling and CO2 interrogate distinct vascular regulations

Neurovascular coupling (NVC), which mediates rapid increases in cerebral blood flow in response to neuronal activation, is commonly used to map brain activation or dysfunction. Here we tested the reemerging hypothesis that CO<sub>2</sub> generated by neuronal metabolism contributes to NVC. We combined functional ultrasound and two-photon imaging in the mouse barrel cortex to specifically examine the onsets of local changes in vessel diameter, blood flow dynamics, vascular/perivascular/intracellular pH, and intracellular calcium signals along the vascular arbor in response to a short and strong CO<sub>2</sub> challenge (10 s, 20%) and whisker stimulation. We report that the brief hypercapnia reversibly acidifies all cells of the arteriole wall and the periarteriolar space 3-4 s prior to the arteriole dilation. During this prolonged lag period, NVC triggered by whisker stimulation is not affected by the acidification of the entire neurovascular unit. As it also persists under condition of continuous inflow of CO<sub>2</sub>, we conclude that CO<sub>2</sub> is not involved in NVC.

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Publication Details

Journal
Nature Communications
Published
2024-09-02
DOI
https://doi.org/10.1038/s41467-024-49698-9
Citations
20
Primary Topic
Traumatic Brain Injury and Neurovascular Disturbances
Type
article
Field-Weighted Citation Impact
7.38

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article

Neurovascular coupling and CO2 interrogate distinct vascular regulations

Anne Joutel, Emmanuelle Chaigneau, Jessica A. Filosa, Ali-Kemal Aydin et al.
20 citations
Nature Communications
Traumatic Brain Injury and Neurovascular Disturbances
7.38
article

Neurovascular coupling and CO2 interrogate distinct vascular regulations

Anne Joutel, Emmanuelle Chaigneau, Jessica A. Filosa, Ali-Kemal Aydin, Serge Charpak, Yannick Goulam Houssen, Marine Tournissac, Sonia Pfister, Mayeul Collot, Philip O’Herron
article en
20 citations

Abstract

Neurovascular coupling (NVC), which mediates rapid increases in cerebral blood flow in response to neuronal activation, is commonly used to map brain activation or dysfunction. Here we tested the reemerging hypothesis that CO<sub>2</sub> generated by neuronal metabolism contributes to NVC. We combined functional ultrasound and two-photon imaging in the mouse barrel cortex to specifically examine the onsets of local changes in vessel diameter, blood flow dynamics, vascular/perivascular/intracellular pH, and intracellular calcium signals along the vascular arbor in response to a short and strong CO<sub>2</sub> challenge (10 s, 20%) and whisker stimulation. We report that the brief hypercapnia reversibly acidifies all cells of the arteriole wall and the periarteriolar space 3-4 s prior to the arteriole dilation. During this prolonged lag period, NVC triggered by whisker stimulation is not affected by the acidification of the entire neurovascular unit. As it also persists under condition of continuous inflow of CO<sub>2</sub>, we conclude that CO<sub>2</sub> is not involved in NVC.

Nature CommunicationsVol. 15(1)
Centre National de la Recherche Scientifique (FR), Institut de la Vision (FR), Inserm (FR), Université Paris Cité (FR), Augusta University (US), Sorbonne Université (FR), Institut de Psychiatrie et Neurosciences de Paris (FR), Université de Strasbourg (FR)
Agence Nationale de la Recherche, Fondation Leducq, Institut National de la Santé et de la Recherche Médicale, Fondation pour la Recherche Médicale, FONDATION ALZHEIMER, National Institutes of Health
Openalex Percentile: Top 2%
Traumatic Brain Injury and Neurovascular Disturbances
7.38
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