The Cerebral Metabolic Consequences of Nitric Oxide Synthase Deficiency: Glucose Utilization in Endothelial and Neuronal Nitric Oxide Synthase Null Mice

Author:

Browne Susan E.1,Ayata Cenk2,Huang Paul L.3,Moskowitz Michael A.2,Beal M. Flint1

Affiliation:

1. Laboratory of Neurochemistry, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusettes, U.S.A.

2. Stroke and Neurovascular Regulation, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusettes, U.S.A.

3. Cardiovascular Research Center, Neurology Service, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusettes, U.S.A.

Abstract

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, CS7B1/6). 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.

Publisher

SAGE Publications

Subject

Cardiology and Cardiovascular Medicine,Clinical Neurology,Neurology

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