Abstract
The study was conducted to investigate the effect of serotonin depletion on nitric oxide-induced meningeal vascular response and cerebrovascular nociception. Nitroglycerin was infused i.v. to control and serotonin-depleted rats. Pial circulation was monitored by intravital fluorescent videomicroscopy and Fos immunoreactivity trigeminal nucleus caudalis neurons was used as an indicator for the cerebrovascular nociception. The results showed that the degree of nitric oxide-induced pial microvascular dilatation was significantly greater in the serotonin-depleted group than the control. The number of nitric oxide-evoked Fos-immunoreactive cells between the two groups remained comparable. The results suggest that though depletion of serotonin can facilitate the vascular response to nitric oxide it does not alter the nitric oxide-induced craniovascular nociceptive response.
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