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The Blood Oxygenation Level-Dependent (BOLD) activation reflects hemodynamic events mediated by neurovascular coupling. During task performance, the BOLD hemodynamic response in a relevant area is mainly driven by the high levels of synaptic activity (reflected in local field potentials, LFP) but, in contrast, during a task-free, resting state, the contribution to BOLD of such neural events is small, as expected by the comparatively (to the task state) low level of neural events. Concomitant recording of BOLD and LFP at rest in animal experiments has estimated the neural contribution to BOLD to ~10%. Such experiments have not been performed in humans. As an approximation, we recorded (in the same subject, N = 57 healthy participants) at a task-free, resting state the BOLD signal and, in a different session, the magnetoencephalographic (MEG) signal, which reflects purely neural (synaptic) events. We then calculated the turnover of these signals by computing the successive moment-to-moment difference in the BOLD and MEG time series and retaining the median of the absolute value of the differenced series (TBOLD and TMEG, respectively). A linear regression of normalized TBOLD vs. TMEG revealed that ~30% of TMEG contributes to TBOLD, accounting for 11.3% of the latter's variance. This percentage estimate is close to the ~10% estimate above obtained by direct recordings in animal experiments.
Georgopoulos et al. (Wed,) studied this question.