Cerebral Cortex Advance Access first published online on March 6, 2008
This version published online on March 10, 2008
Cerebral Cortex, doi:10.1093/cercor/bhn023
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The Influence of Moderate Hypercapnia on Neural Activity in the Anesthetized Nonhuman Primate
1
urbil1,21 Max-Planck Institute for Biological Cybernetics, Spemannstrasse 38, 72076 Tübingen, Germany, 2 Center for Magnetic Resonance Research University of Minnesota, Minneapolis, MN 55416, USA, 3 Imaging Science and Biomedical Engineering, University of Manchester, Manchester, UK
Address correspondence to Anne-Catherin Zappe, Max-Planck Institute for Biological Cybernetics, Spemannstr 38, 72076 Tübingen, Germany. Email: aczappe{at}tuebingen.mpg.de.
Hypercapnia is often used as vasodilatory challenge in clinical applications and basic research. In functional magnetic resonance imaging (fMRI), elevated CO2 is applied to derive stimulus-induced changes in the cerebral rate of oxygen consumption (CMRO2) by measuring cerebral blood flow and blood-oxygenation-level–dependent (BOLD) signal. Such methods, however, assume that hypercapnia has no direct effect on CMRO2. In this study, we used combined intracortical recordings and fMRI in the visual cortex of anesthetized macaque monkeys to show that spontaneous neuronal activity is in fact significantly reduced by moderate hypercapnia. As expected, measurement of cerebral blood volume using an exogenous contrast agent and of BOLD signal showed that both are increased during hypercapnia. In contrast to this, spontaneous fluctuations of local field potentials in the beta and gamma frequency range as well as multiunit activity are reduced by
15% during inhalation of 6% CO2 (pCO2 = 56 mmHg). A strong tendency toward a reduction of neuronal activity was also found at CO2 inhalation of 3% (pCO2 = 45 mmHg). This suggests that CMRO2 might be reduced during hypercapnia and caution must be exercised when hypercapnia is applied to calibrate the BOLD signal.
Key Words: cerebral cortex extracellular recording fMRI macaque metabolism neurovascular coupling striate cortex