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Am J Physiol Regul Integr Comp Physiol 277: R1760-R1770, 1999;
0363-6119/99 $5.00
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Vol. 277, Issue 6, R1760-R1770, December 1999

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

Guang Yang1, Gang Chen2, Timothy J. Ebner2, and Costantino Iadecola1,2

1 Laboratory of Cerebrovascular Biology and Stroke, Departments of Neurology and 2 Neuroscience, University of Minnesota Medical School, Minneapolis, Minnesota 55455

Crus II is an area of the cerebellar cortex that receives trigeminal afferents from the perioral region. We investigated the mechanisms of functional hyperemia in cerebellum using activation of crus II by somatosensory stimuli 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 measured by laser-Doppler flowmetry. Crus II was activated by electrical stimulation of the perioral region (upper lip). Perioral stimulation evoked the characteristic field potentials in crus II and increased BFcrb (34 ± 6%; 10 Hz-25 V; n = 6) without changing arterial pressure. The BFcrb increases were 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 µM; P < 0.01; n = 5). The neuronal NO synthase inhibitor 7-nitroindazole (7-NI, 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 contrast, 7-NI attenuated the increase in neocortical cerebral blood flow produced by perioral stimulation by 52 ± 6% (P < 0.05; n = 5). We conclude that crus II activation by somatosensory stimuli produces localized increases in local neural activity and BFcrb that are mediated by activation of glutamate 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 cerebellum.

cerebral circulation; laser-Doppler flowmetry; glucose utilization; vasodilation; glutamate receptors


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