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Volume 151, Issue 2, Pages 90-97 (3 December 2009)


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Localization of NADPH oxidase in sympathetic and sensory ganglion neurons and perivascular nerve fibers

Xian Caoab1, Stacie L. Demelad1, Mark T. Quinne, James J. Galliganad, David KreulenabcCorresponding Author Informationemail address

Received 24 September 2008; received in revised form 8 June 2009; accepted 10 July 2009.

Abstract 

Superoxide anion (O2−•) production was previously reported to be increased in celiac ganglia (CG) during DOCA–salt hypertension, possibly via activation of the reduced nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase. This suggested a role for neuronal NADPH oxidase in autonomic neurovascular control. However, the expression and localization of NADPH oxidase in the peripheral neurons are not fully known. The purpose of this study was to examine the subcellular localization of NADPH oxidase in sympathetic and sensory ganglion neurons and perivascular nerve fibers. In rat CG, p22phox and neuropeptide Y (NPY) were colocalized in all neurons. P22phox was also localized to dorsal root ganglia (DRG) neurons that contain calcitonin gene related peptide (CGRP). In mesenteric arteries, p22phox and p47phox were colocalized with NPY or CGRP in perivascular nerve terminals. A similar pattern of nerve terminal staining of p22phox and p47phox was also found in cultured CG neurons and nerve growth factor (NGF)-differentiated PC12 cells. These data demonstrate a previously uncharacterized localization of NADPH oxidase in perivascular nerve fibers. The presence of a O2−•-generating enzyme in close vicinity to the sites of neurotransmitter handling in the nerve fibers suggests the possibility of novel redox-mediated mechanisms in peripheral neurovascular control.

a The Neuroscience Program, Michigan State University, East Lansing, MI 48824, United States

b Department of Physiology, Michigan State University, East Lansing, MI 48824, United States

c Department of Neurology and Ophthalmology, Michigan State University, East Lansing, MI 48824, United States

d Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, United States

e Department of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, United States

Corresponding Author InformationCorresponding author. Department of Physiology, 2201 Biomedical Physical Sciences, Michigan State University, East Lansing, MI 48824, United States. Tel.: +1 517 355 6475; fax: +1 517 355 5125.

1 Contributed equally to this work.

PII: S1566-0702(09)00408-1

doi:10.1016/j.autneu.2009.07.010


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