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要旨

Recent evidence suggests that increased metabolic demand of neurons can be met by lactate, a metabolite of glucose. In addition, during neuronal activation lactate production in the brain is increased. We already demonstrated that this physiological formation of lactate can contribute to the BOLD signal. Here we set out to determine the underlying mechanism that drives the observed increase in BOLD baseline. This effect could be explained by an increase in CBF or also increased neuronal activity. The influence of lactate on cerebral blood flow has been already established. To test if lactate has also an effect on neuronal activity we performed electrophysiological recordings in V1 of anesthetized non-human primates. Lactate was applied slow and continuously (0.04 mmol/kg/min). This infusion induced a significant increase in local field potential (LfpH, 24-90 Hz) power and visual stimulus induced modulation. An average increase of 23.0±1.2 and 76.0±20 was recorded for power and modulation of LfpH respectively; this effect reached significance 4.8±3.1 min after the start of the injection and lasted for 19.5±5.0 min. The timing of the effects is comparable to the timing of the BOLD signal increase evoked by the same infusion protocol of lactate. In the multiunit activity (MUA, 400-3000 Hz) no significant effect was observed. In summary, by applying lactate, a potential fuel for activated neurons, we increase LfpH power and modulation but not the spiking activity. Since LfpH is a reliable driver of the BOLD signal at least part of the lactate effect on the BOLD signal can be explained by an increase in neuronal activity.