Abstract
Neural activities trigger an increase in local cerebral blood flow (CBF). However, it is unclear how this "coupling" is mediated. Recently, it is proposed that prostanoids and nitric oxide (NO) may serve as vasodilators in the activity-dependent changes in CBF. We investigated this hypothesis with functional brain imaging using flavoprotein autofluorescence. We anesthetized C57BL/6N mice with urethane (1.7 g/kg, i.p) and exposed the skull. The surface of the skull was covered with clear acrylic resin for preventing drying and keeping the transparency of the skull. Cortical images of green autofluorescence (500-550 nm) in blue light (450-490 nm) were recorded through the intact skull at 9 Hz by a cooled CCD camera system attached to an epifluorescence microscope. Neural activities in the primary somatosensory cortex were elicited by vibratory stimulation at 50 Hz for 1 s applied on the contralateral hind paw skin. An activity-dependent increase in the autofluorescence was observed and followed by darkening of the arterial images reflecting vasodilation. Indomethacin (10 mg/kg, i.p) weakly attenuated the arterial darkening without changing neural responses. L-NAME (30 mg/kg, i.p), a nonspecific NOS inhibitor, did not modify neural responses and the arterial darkening by itself. However, co-application of indomethacin and L-NAME almost completely eliminated the arterial darkening, and activity-dependent vasoconstriction was observed instead. These data suggest that prostanoids and NO mediate activity dependent changes in CBF. [Jpn J Physiol 54 Suppl:S144 (2004)]
