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Abstract:
The underlying neurophysiological source of the BOLD signal is still not fully understood. The spike rate of single neurons is only poorly correlated with the time course of the BOLD signal. The BOLD signal seems rather to reflect the activity of the presynaptic network the neurons are embedded in. We therefore blocked the neuronal activity in a defined area with lidocaine, a reversible sodium channel blocker. In this way we could investigate, how the BOLD signal is coupled to the neuronal activity.
The effects were assessed by simultaneous intracortical recordings and fMRI. We examined BOLD responses in regions of interest defined by independent localizer scans, and assessed the spatial effect of the blocker at varying distances from the injection site.
Neuroimaging was performed in a 4.7 Tesla Scanner. We recorded multiunit activity (MUA) and local field potentials (LFPs). V1 was stimulated by rotating polar checkerboard stimulus. At a distance of 400 microns to the recording electrode we injected Lidocaine (2-6). Applied quantities (5-25 microl) and flow rates (0.8-4 microl /min) were monitored by a flow meter.
Lidocaine injections were associated with reliable decreases in neuronal activity and local decreases in BOLD activity. Both neuronal and BOLD signals recovered at a timescale of several minutes. However, early in the recovery phase there was a clear transient increase in the gamma band LFP, while the MUA activity was still blocked. The BOLD signal showed a stimulus-modulated increase due to recovery, which however paralled neither the transient increase in LFP nor the still unmodulating MUA signal. The early period in the recovery from lidocaine inactivation thus represents a cortical state in which BOLD signal levels are largely decoupled from the neuronal ones. Our findings suggest that even general blockers (lidocaine) can generate interesting states of neurovascular decoupling that can be used for a better understanding of the BOLD signal.
