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Pain Research and Treatment
Volume 2012, Article ID 414697, 9 pages
Research Article

Glutaminase Immunoreactivity and Enzyme Activity Is Increased in the Rat Dorsal Root Ganglion Following Peripheral Inflammation

1Department of Anatomy and Cell Biology, Oklahoma State University Center for Health Sciences, Tulsa, OK 74107, USA
2Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73190, USA
3Tulsa Bone & Joint Associates, Tulsa, OK 74146, USA
4Department of Anatomical Sciences & Neurobiology, University of Louisville School of Medicine, Louisville, KY 40202, USA
5Affiliated Dermatology, Scottsdale, AZ 85255, USA
6Department of BioMedical Sciences, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA

Received 1 July 2011; Revised 29 August 2011; Accepted 8 September 2011

Academic Editor: Paul G. Green

Copyright © 2012 Kenneth E. Miller et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Following inflammation, primary sensory neurons in the dorsal root ganglion (DRG) alter the production of several proteins. Most DRG neurons are glutamatergic, using glutaminase as the enzyme for glutamate production, but little is known about glutaminase following inflammation. In the present study, adjuvant-induced arthritis (AIA) was produced in rats with complete Freund's adjuvant into the hindpaw. At 7 days of AIA, DRG were examined with glutaminase immunohistochemistry, Western blot immunoreactivity, and enzyme activity. Image analysis revealed that glutaminase was elevated most in small-sized neurons (21%) (P < 0.05). Western blot analysis revealed a 19% increase (P < 0.05) in total glutaminase and 21% in mitochondrial glutaminase (P < 0.05). Glutaminase enzyme activity was elevated 29% (P < 0.001) from 2.20 to 2.83 moles/kg/hr. Elevated glutaminase in primary sensory neurons could lead to increased glutamate production in spinal primary afferent terminals contributing to central sensitization or in the peripheral process contributing to peripheral sensitization.