Nitric oxide is the predominant mediator of cerebellar hyperemia during somatosensory activation in rats

Crus II is an area of the cerebellar cortex that receives trigeminal affere nts from the perioral region. We investigated the mechanisms of functional hyperemia in cerebellum using activation of crus II by somatosensory stimul i as a model. In particular, we sought to determine whether stimulation of the perioral, region increases cerebellar blood flow (BFcrb) in crus II and , if so, whether the response depends on activation of 2-amino-3-hydroxy-5- methylisoxazole-4-propionic acid (AMPA)-kainate receptors and nitric oxide (NO) production. Crus II was exposed in anesthetized rats, and the site was superfused with Ringer. Field potentials were recorded, and BFcrb was meas ured by laser-Doppler flowmetry. Crus II was activated by electrical stimul ation of the perioral region (upper Lip). Perioral stimulation evoked the c haracteristic field potentials in crus II and increased BFcrb (34 +/- 6%; 1 0 Hz-25 V; n = 6) without changing arterial pressure. The BFcrb increases w ere associated with a local increase in glucose utilization (74 +/- 8%; P < 0.05; n = 5) and were attenuated by the AMPA-kainate receptor antagonist 2 ,3-dihydroxy-6-nitro-7-sulfamoylbenzo-[f]quinoxaline (-71 +/- 3%; 100 mu M; P < 0.01; n. = 5). The neuronal NO synthase inhibitor 7-nitroindazole (7-N I, 50 mg/kg; n = 5) virtually abolished the increases in BFcrb (-90 +/- 2%; P < 0.01) but did not affect the amplitude of the field potentials. In con trast, 7-NI attenuated the increase in neocortical cerebral blood flow prod uced by perioral stimulation by 52 +/- 6% (P < 0.05; n = 5). We conclude th at crus II activation by somatosensory stimuli produces localized increases in local neural activity and BFcrb that are mediated by activation of glut amate receptors and NO. Unlike in neocortex, in cerebellum the vasodilation depends almost exclusively on NO. The findings underscore the unique role of NO in the mechanisms of synaptic function and blood flow regulation in c erebellum.