Implication of Nitric Oxide Synthase in Radiation-Induced Decrease in HippocampalNoradrenaline Release in Rats

摘要

The hippocampus is important in critical functions such as learning, memory, andmotor performance, and these functions are impaired after exposure to ionizing radiation. Noradrenergic systems are important in mediating arousal, food intake and to some extent motor functions; histofluorescence and immunohistochemical techniques have shown noradrenergic pathways in the hippocampus. Several factors can contribute to acute nervous system damage in vivo: systemic blood pressure is reduced following exposure to 25-100 Gy gamma radiation and cerebral blood flow decreases in a variety of brain regions, including the hippocampus; the ischaemia produced by decreased blood flow is likely to affect neuronal activity; ionizing radiation generates free radicals, and resulting oxygen radicals have been implicated in cell damage following ischaemia; brain ischaemia induces the release of an excessive amount of glutamate in the hippocampus, and glutamate acts on nitric oxide (NO) synthase to form NO through N-methyl-D-aspartate receptors, causing toxic effects. The purpose of this study was to examine the effect of ionizing radiation on hippocampal noradrenaline (NA) release in vitro, stimulated by KCl 0.5, 24, 48, and 72 h after irradiation/sham-irradiation and to determine th role of NO synthase in the radiation-induced decrease in NA release.