SOMATOSENSORY SYSTEMS, PAINNitric oxide in hyperbaric oxygen-induced acute antinociception in miceOhgami, Yusukea; Zylstra, Carlyn C.a; Quock, Lindsay P.a; Chung, Eunheea; Shirachi, Donald Y.c; Quock, Raymond M.a bAuthor Information aDepartment of Pharmaceutical Sciences, College of Pharmacy bCenter for Integrated Biotechnology, Washington State University, Pullman, Washington cChico Hyperbaric Center, Chico, California, USA Correspondence to Dr Raymond M. Quock, Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, PO Box 646534, Pullman, WA 99164, USA Tel: +1 509 335 5956; fax: +1 509 335 5902; e-mail: email@example.com Received 26 May 2009 accepted 1 July 2009 NeuroReport: October 7th, 2009 - Volume 20 - Issue 15 - p 1325-1329 doi: 10.1097/WNR.0b013e3283305a49 Buy SDC Metrics Abstract Hyperbaric oxygen (HBO2) therapy induces analgesia in various conditions of pain in humans. In mice, HBO2 treatment evokes an acute antinociceptive response in the abdominal constriction test. To demonstrate the dependence of HBO2-induced antinociception on nitric oxide (NO), antinociceptive responsiveness to HBO2 was assessed after three different approaches that interfered with NO production. HBO2-induced antinociception was significantly attenuated by intracerebroventricular and intrathecal pretreatment with an inhibitor of NO synthase (NOS) enzyme and also by an antisense oligodeoxynucleotide directed against neuronal NOS. The antinociceptive effect was also significantly reduced in mice homozygous for a defective neuronal NOS gene. On the basis of these results, we conclude that neuronal NO is critical in the expression of the acute antinociceptive effect of HBO2. © 2009 Lippincott Williams & Wilkins, Inc.