Functional Uncoupling of Hemodynamic from Neuronal Response by Inhibition of Neuronal Nitric Oxide Synthase

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  • Bojana Stefanovic
    Cerebral Microcirculation Unit, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA
  • Wolfram Schwindt
    Department of Clinical Radiology, University Hospital Münster, Münster, Germany
  • Mathias Hoehn
    In-vivo-NMR-Laboratory, Max-Planck-Institute for Neurological Research, Cologne, Germany
  • Afonso C Silva
    Cerebral Microcirculation Unit, Laboratory of Functional and Molecular Imaging, National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA

説明

<jats:p> The cerebrovascular coupling under neuronal nitric oxide synthase (nNOS) inhibition was investigated in α-chloralose anesthetized rats. Cerebral blood flow (CBF), cerebral blood volume (CBV), and blood oxygenation level dependent (BOLD) responses to electrical stimulation of the forepaw were measured before and after an intraperitoneal bolus of 7-nitroindazole (7-NI), an in vivo inhibitor of the neuronal isoform of nitric oxide synthase. Neuronal activity was measured by recording somatosensory-evoked potentials (SEPs) via intracranial electrodes. 7-Nitroindazole produced a significant attenuation of the activation-elicited CBF ( P < 10<jats:sup>−6</jats:sup>), CBV ( P < 10<jats:sup>−6</jats:sup>), and BOLD responses ( P < 10<jats:sup>−6</jats:sup>), without affecting the baseline perfusion level. The average Δ CBF was nulled, while Δ BOLD and Δ CBV decreased to ~30% of their respective amplitudes before 7-NI administration. The average SEP amplitude decreased ( P < 10<jats:sup>−5</jats:sup>) to ~60% of its pretreatment value. These data describe a pharmacologically induced uncoupling between neuronal and hemodynamic responses to functional activation, and provide further support for the critical role of neuronally produced NO in the cerebrovascular coupling. </jats:p>

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