We are interested in studying how biochemical changes in the brain contribute to anxiety disorders. Our primary focus is to investigate a potentially causal role of oxidative stress in these disorders. Behavioral, pharmacological, biochemical and immunohistochemical approaches in neuronal cell culture and rodent models of oxidative stress are utilized to examine mechanistic underpinnings of anxiety disorders. Involvement of oxidative stress in comorbid prevalence of anxiety disorders with cognitive impairment and hypertension, also are being explored. Current research projects in my laboratory include a National Institute of Mental Health (NIMH) funded project, which is focused on determining role of antioxidant defense mechanism mediated by a Regulator of G-Protein Signaling Protein (RGS)-2 in anxiety-like behavior of rats. Involvement of PKC, p38 MAPK and calpains in regulation of these mediators specifically involvement of antioxidant defense enzymes including glutathione reductase 1 and glyoxalase 1 in anxiety-like behavior of rats is being examined. Our recent work has identified that induction of oxidative stress via pharmacological intervention or via induction of psychological stress of acute sleep-deprivation, both lead to anxiety-like behavior in rats. We also have observed a causal role of oxidative stress in hypertension, and learning and memory impairment in rats. Projects are underway to investigate a deeper understanding of the underlying biology of some of these debilitating disorders.
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