CO 2 breathing Suppresses Cerebral Metabolic Rate of Oxygen

INTRODUCTION: CO2 has been known for its high potency in modulating blood flow. However the effect of CO2 on neuronal activity and brain energy consumption is not yet known. Characterization of such an effect can provide a new opportunity to non-invasively and conveniently modulate neural activity in humans, which traditionally would have to be done surgically or transcranially. For example, suppressing of neural activity can be used to terminate an epileptic episode (1). Also, the ability of reducing neural activity may provide a potential therapy for insomnia and other sleep disorders. In addition, understanding the effect of CO2 on neurons is useful in re-assessing CO2 as a pure vascular challenge as well as in interpreting the data of calibrated fMRI studies. A recent electroneurophysiology study in anesthetized animal provided evidences that mild hypercapnia (HC) reduces neural activity (2). Here we performed an MRI and an EEG study to assess the effect of HC on oxygen consumption and neural activity in humans. In the MRI study, we used a recently developed method (3) to measure cerebral metabolic rate of oxygen (CMRO2) during normocapnia (NC) and HC. In the EEG study, we measured surface electrode potentials during NC and HC. METHODS: MRI experiments (8 healthy controls, 5 M, 3 F, age 20-35) were performed on a 3T Philips System. Absolute CMRO2 in units of μmol/min was calculated using Fick principle 2 ( ) a v a CMRO CBF Y Y C = ⋅ − ⋅ , where CBF is the blood flow in ml/min, Ya is the arterial oxygenation (%), Yv is the