Abstract
The role of nitric oxide (NO) in the pathogenesis of cerebral disorders is poorly understood (Bruhwyler et al., 1993; Choi, 1993). Many reports suggest that brain damage caused by excessive release of excitatory amino acids is mediated by NO formation (Dawson et al., 1991; Nowicki et al., 1991; Buisson et al., 1993). But there are conflicting findings which show that NO can function rather as a protective agent (Yamamoto et al., 1992; Weissmann et al., 1992). Moreover, the contribution of glial cells to the NO production in intact and damaged brain tissue is quite unclear. Choi (1993) has recently summarized the current discussion concluding that “a plethora of variables and the inherent complexity of NO biology hinder present efforts to define the effects of NO upon the injured brain”.
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Wolf, G., Schmidt, W., Calka, J., Henschke, G., Würdig, S. (1995). Brain Lesion and Nitric Oxide Synthase/Nadph-Diaphorase: a Light and Electron Microscopical Study. In: Weissman, B.A., Allon, N., Shapira, S. (eds) Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1903-4_26
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DOI: https://doi.org/10.1007/978-1-4615-1903-4_26
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