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.
D000818:Animals; D001931:Brain Mapping; D002415:Cats; D002531:Cerebellum / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology*; D002560:Cerebrovascular Circulation / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D004734:Energy Metabolism / Q000187:drug effects / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007839:Functional Laterality / Q000502:physiology; D005947:Glucose / Q000378:metabolism; D007191:Indazoles / Q000494:pharmacology; D008297:Male; D009474:Neurons / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D013003:Somatosensory Cortex / Q000000981:diagnostic imaging / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014055:Tomography, Emission-Computed; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
D004791:Enzyme Inhibitors; D007191:Indazoles; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D005947:Glucose; C080122:7-nitroindazole