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Poster

The effect of lidocaine on neural activity and BOLD activity in monkey primary visual cortex

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons84158

Rauch,  A
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons83787

Augath,  M
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons84733

Oeltermann,  A
Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons84154

Rainer,  G
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons84063

Logothetis,  NK
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Zitation

Rauch, A., Augath, M., Oeltermann, A., Rainer, G., & Logothetis, N. (2005). The effect of lidocaine on neural activity and BOLD activity in monkey primary visual cortex. Poster presented at 35th Annual Meeting of the Society for Neuroscience (Neuroscience 2005), Washington, DC, USA.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0013-D3D1-9
Zusammenfassung
The neurophysiological basis of BOLD contrast mechanism in fMRI is not fully understood. Therefore we started to investigate the role of different neuromodulators and channel blockers on the neural and hemodynamic responses. We first report the effects of local injection of Lidocaine, a reversible sodium channel blocker, in primary visual cortex (V1) of anesthetized monkeys. 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 (Bruker, Germany). Recorded were spiking activity and local field potentials. V1 was stimulated by rotating polar checkerboard stimulus (blocks by 30 sec stimulus, 30 sec blank, 37 repetitions). 300 μm to the recording electrode we injected Lidocaine (2 solution) with a precision pump (M6 VICI, USA). Applied quantities (8-25 μl) and flow rates (0.8-4 μl /min) were monitored by a precision flow meter (Sensirion, Switzerland). Consistent with previous reports, Lidocaine induced reliable decreases in neuronal activity at the injection site. In addition, we observed clear decreases in BOLD activity. The largest effect on both signals was observed closest to the injection site and decreased with increasing distance. The effect was reversible for both signals with a recovery time of 20-30 minutes. Injection of saline (0.9), to rule out nonspecific effects, showed no change in neuronal or BOLD signals. The findings suggest a close coupling between stimulus-evoked neuronal activity and the BOLD signal. This allows for a better quantification of the primarily interesting part of the BOLD signal involved in neuronal processing as we now can distinguish between the BOLD signal needed for information processing and the portion used for homeostasis of neurons and their embedding glial cells.