NeurochemistryIncreased nitric oxide synthase in the vasculature of the epaulette shark brain following hypoxiaC. Renshaw, Gillian M.1,3; Dyson, Susan E.2Author Information 1Department of Anatomical Sciences, University of Queensland, St Lucia 4072, Queensl. 4072, Australia 2Department of Anatomy and Human Biology, University of Western Australia, Nedlands 6001, WA, Australia 3Corresponding Author: Gillian M. C. Renshaw ACKNOWLEDGEMENTS: We thank Sea World Research and Rescue foundation for funding this project, the staff of Heron Island Research Station for their assistance, Colin McQueen for his invaluable help with the confocal microscopy and Chris Kerrisk for excellent propidium iodide staining. Received 23 March 1999; accepted 13 April 1999 NeuroReport: June 3rd, 1999 - Volume 10 - Issue 8 - p 1707-1712 Buy Abstract EPAULETTE sharks inhabiting reef platforms are exposed to hypoxic and hyperoxic cycles. The adaptive mechanisms used to prevent neurological damage during these cycles have not been examined. Nitric oxide has a neuroprotective role in some hypoxia-tolerant species. We examined epaulette brains following a severe experimental hypoxic regimen (0.39 mgO2+l for 2 h) and compared nitric oxide synthase (NOS) expression with that in normoxic controls using NADPH-diaphorase staining. Intense NOS activity occurred in microvasculature following exposure to a severely hypoxic environment in contrast to the low levels seen in controls. We established for the first time that the epaulette shark was hypoxia-tolerant because there was no delayed phase of neuronal apoptosis. Enhanced NOS production in response to hypoxia may cause vasodilation, which would maintain the appropriate metabolic environment for continued neuronal survival during exposure to hypoxia. © 1999 Lippincott Williams & Wilkins, Inc.