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Free keywords:
Endothelium; Cerebral circulation; Laser-Doppler; Somatosensory stimulation; Rat
Abstract:
We tested the hypothesis that nitric oxide (NO) is a mediator in the coupling of cerebral blood flow to neuronal activation. The production of NO was blocked in anesthetized rats with the NO-synthase inhibitor (l-NA). In controls, vibrissae stimulation for 60 s led to a fast (≤ 2 s), 17% increase in regional cerebral blood flow (rCBF) in the contralateral somatosensory cortex. Systemical (10 mg/kg) as well as topical (10−3 M) application of l-NA reduced the response to stimulation by approximately 50%. Systemical application primarily attenuated the early component of the response, whereas topical application led to an attenuation throughout the whole 60-s stimulation interval. We conclude that NO is involved in rCBF coupling to neuronal activation.
