Why the study?
Does deficiency of endothelial or neuronal nitric oxide synthase alter local cerebral glucose utilization in mice?
Does deficiency of endothelial or neuronal nitric oxide synthase alter local cerebral glucose utilization in mice?
Deficiency of endothelial or neuronal nitric oxide synthase does not significantly alter cerebral glucose utilization compared to C57B1/6 wild-type mice.
nNOS/eNOS deficiency does not alter cerebral glucose utilization in mice; leaves open strain-specific or pathological effects for future study.
Nitric oxide has multiple physiologic roles in the CNS. Inhibiting nitric oxide synthesis might therefore alter functional activity within the brain. We used [14C]-2-deoxyglucose in vivo autoradiography to measure local CMRglc in "knockout" mice lacking the genes for either the endothelial (eNOS) or neuronal (nNOS) isoforms of nitric oxide synthase, and in the progenitor strains (SV129, C57B1/6). Glucose utilization levels did not significantly differ between nNOS and eNOS knockout mice and C57B1/6 mice in any of the 48 brain regions examined, but were relatively lower in some subcortical regions in SV129 mice.
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Browne et al. (1999) studied this question.
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