Original Research ARTICLE

Front. Neuroenergetics, 18 November 2009 | http://dx.doi.org/10.3389/neuro.14.007.2009

The possible role of CO2 in producing a post-stimulus CBF and BOLD undershoot

Institute of Biomedical Engineering, Boǧaziçi University, Istanbul, Turkey
HMS/MIT/MGH Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, MA, USA
Department of Neurosciences, University of California San Diego, La Jolla, CA, USA
Comprehending the underlying mechanisms of neurovascular coupling is important for understanding the pathogenesis of neurodegenerative diseases related to uncoupling. Moreover, it elucidates the casual relation between the neural signaling and the hemodynamic responses measured with various imaging modalities such as functional magnetic resonance imaging (fMRI). There are mainly two hypotheses concerning this mechanism: a metabolic hypothesis and a neurogenic hypothesis. We have modified recent models of neurovascular coupling adding the effects of both NO (nitric oxide) kinetics, which is a well-known neurogenic vasodilator, and CO2 kinetics as a metabolic vasodilator. We have also added the Hodgkin–Huxley equations relating the membrane potentials to sodium influx through the membrane. Our results show that the dominant factor in the hemodynamic response is NO, however CO2 is important in producing a brief post-stimulus undershoot in the blood flow response that in turn modifies the fMRI blood oxygenation level-dependent post-stimulus undershoot. Our results suggest that increased cerebral blood flow during stimulation causes CO2 washout which then results in a post-stimulus hypocapnia induced vasoconstrictive effect.
carbon dioxide, nitric oxide, cerebral blood flow, vasodilation, CMRO2, fMRI
Yücel MA, Devor A, Akin A and Boas DA (2009). The possible role of CO2 in producing a post-stimulus CBF and BOLD undershoot. Front. Neuroenerg. 1:7. doi: 10.3389/neuro.14.007.2009
08 June 2009;
 Paper pending published:
17 July 2009;
08 October 2009;
 Published online:
18 November 2009.

Edited by:

Bruno Weber, University of Zurich, Switzerland

Reviewed by:

Kamil Uludaǧ, Max Planck Institute, Germany
Fahmeed Hyder, Yale University, USA
© 2009 Yücel, Devor, Akin and Boas. This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.
David A. Boas, Harvard Medical School, 13th Street Building 149, Charlestown, MA 02129, USA. e-mail: dboas@nmr.mgh.harvard.edu