Neuronal nitric oxide has a role as a perfusion regulator and a synaptic modulator in cerebellum but not in neocortex during somatosensory stimulation--an animal PET study.

To clarify a role of neuronal nitric oxide in neurovascular coupling, we performed cerebral blood flow (CBF) and cerebral metabolic rate of glucose (CMR(glc)) measurements with positron emission tomography in somatosensory-stimulated cats using a specific neuronal nitric oxide synthase inhibitor, 7-nitroindazole (7-NI). The effect on flow-metabolism coupling were tested by global and regional-specific changes on CBF and CMR(glc), and the regional-specific effect was estimated both by regions of interest (ROI) and voxel-based (VB) analysis using globally-normalized CBF and CMR(glc) changes. The electrical somatosensory stimulation in the unilateral forepaw elicited coupled increase in CBF and CMR(glc) in the contralateral somatosensory cortex (7%) and the ipsilateral cerebellum (8%). 7-NI induced 20% decrease in global CBF both during rest and activation, but not in global CMR(glc) at simulation. Both ROI and VB analysis showed that 7-NI induced an increase in CMR(glc) (13%) in the ipsilateral cerebellum compared to control under vehicle alone, but it was accompanied by only 8% increase in CBF, suggesting uncoupling of flow-metabolism while it induced any perturbations in the contralateral somatosensory cortex. These observations suggest that neuronal nitric oxide has an important role for a mediator of regional neurovascular coupling as well as synaptic modulator in the cerebellum, but less so in the neocortex.