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The role of adenosine in the neurovascular coupling of the BOLD signal in early visual cortex of non-human primates

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http://pubman.mpdl.mpg.de/cone/persons/resource/persons84502

Viswanath,  S
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons84324

Zaldivar,  D
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons84289

von Pföstl,  V
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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/persons84063

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

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Citation

Viswanath, S., Zaldivar, D., von Pföstl, V., Rauch, A., & Logothetis, N. (2012). The role of adenosine in the neurovascular coupling of the BOLD signal in early visual cortex of non-human primates. Poster presented at 13th Conference of the Junior Neuroscientists of Tübingen (NeNA 2012), Schramberg, Germany.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0013-B576-7
Abstract
In this study, CPX, an antagonist of adenosine was used to determine the role of adenosine in uncoupling the vascular and neuronal response observed by the BOLD signal after a strong visual stimulation in primary visual cortex (V1). We systemically and locally applied CPX and pharmacologically manipulated the sensory response in the early visual cortex of anaesthetized macaques. Pharmacological magnetic resonance imaging (phMRI) in combination with electrophysiology was used to determine the impact of CPX on V1. Results were obtained from recordings of the BOLD and electrophysiological activity during the injections. Systemic application of CPX resulted in a disruption of the visual modulation in the BOLD signal. Local applications of CPX resulted in a decrease in the power of low LFP and an increase in the power of MUA. In addition it resulted in a decrease in the CV and FF. No significant changes were observed in the BOLD signal after systemic application of phosphate buffered saline, which was used as a control. The results show that we indeed observe dissociation between the vascular and the neuronal activity during adenosinergic modulation. Apparently adenosine reduces functional hyperaemia, which is reflected by the reduction in BOLD signal, while underlying neuronal activity is increased, indicated by an increase in MUA. Further studies have to be conducted using simultaneous sampling of neurochemicals and phMRI to fully elucidate the functional role of adenosine for the vascular and neuronal interplay in V1.