Abstract
Summary
NO has clearly revolutionized our thinking about aspects of neurotransmission and neuronal signaling. NO is emerging as an important regulator of a variety of physiologic processes; however, under conditions of excessive or inappropriate formation, NO is also emerging as an important mediator of pathologic nervous tissue damage. Uncovering and understanding the targets of NO that contribute to the neuropathologic process will hopefully lead to the development of selective therapeutic agents and to a better understanding of basic processes underlying normal and pathological neuronal functions.
VLD is supported by grants from USPHS NS22643, NS33142, the American Foundation for AIDS Research, National Alliance for Research on Schizophrenia and Depression, American Heart Association, the Alzheimer's Association and the Muscular Dystrophy Association. T. M. D. is supported by grants from the USPHS NS01578, NS26643, NS33277, and the American Health Assistance Foundation, Paul Beeson Physician Scholars in Aging Research Program and International Life Sciences Institute. The authors own stock in and are entitled to royalty from Guilford Pharmaceuticals, Inc., which is developing technology related to the research described in this article. The stock has been placed in escrow and cannot be sold until a date which has been predetermined by the Johns Hopkins University.
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