In 2008, more than 15 years after the Gulf War had ended, the US Government acknowledged the Gulf War Syndrome as a legitimate illness. That year a congressionally mandated Research Advisory Committee issued a 452-page report that stated, “scientific evidence leaves no question that Gulf War illness is a real condition with real causes and serious consequences for affected veterans. Because it wasn’t acknowledged as an illness there were no significant funds available to research the illness, so next to nothing was known about which brain regions might be involved.
In 2008, my laboratory obtained a VA sponsored contract to study the role of the toxic organophosphate metabolite, chlorpyrifos oxon on various brain regions in order to shed light into the cellular mechanisms of a number of psychological symptoms associated with deployed Gulf War veterans. Over the past few years, we have published a couple papers on the subject. Most recently, (July 8, 2011) we published our most recent findings in Nature Precedings implicating a brain region critically involved in attention, addition and arousal. Visit the site and Vote for our paper and leave us a comment there or at http://www.neuro-cloud.info if you are interested in collaborating with us on this project.
“Gulf War syndrome is a chronic multi-symptom illness that has affected about a quarter of the deployed veterans of the 1991 Gulf War. Exposure to prolonged low-level organophosphate insecticides and other toxic chemicals is now thought to be responsible. Chlorpyrifos was one commonly used insecticide. The metabolite of chlorpyrifos, chlorpyrifos oxon, is a potent irreversible inhibitor of acetylcholinesterase, much like the nerve agent Sarin. To date, the target brain region(s) most susceptible to the neuroactive effects of chlorpyrifos oxon have yet to be identified. To address this we tested ability of chlorpyrifos oxon to influence neuronal excitability and induce lasting changes in the locus coeruleus, a brain region implicated in anxiety, substance use, attention and emotional response to stress. Here we used an ex vivo rodent model to identify a dramatic effect of chlorpyrifos oxon on locus coeruleus noradrenergic neuronal activity. Prolonged exposure to chlorpyrifos oxon caused acute inhibition and a lasting rebound excitatory state expressed after days of exposure and subsequent withdrawal. Our findings indicate that the locus coeruleus is a brain region vulnerable to chlorpyrifos oxon-induced neuroplastic changes possibly leading to the neurological symptoms affecting veterans of the Gulf War.