Abstract
Radiation impairs some functions of the central nervous system, which is one of the radiation-resistant tissues in the body, but the exact mechanisms are still unclear. We found that total body and head, but not abdominal, carbon irradiation induced a significant increase of the release of glutamate, the major excitatory neurotransmitter in the central nervous system, in the hypothalamus. We also found that the increase of glutamate is dependent on the Ca2+ ion, suggesting that the increased glutamate is derived from the release from neurons or glial cells. However, the underlying mechanisms of the increase of glutamate release are still unclear. In this study, we investigated that the effects of the glial selective metabolic inhibitor (L-aminoadipatic acid (L-AA), glutamine synthetase inhibitor (methionine sulfoximide (MSO)) and inhibitor of glutamate release from glial cell (carboxyphenylglycine (CPG)) on the increased glutamate measured by in vivo brain microdialysis. L-AA and MSO completely inhibited the heavy-ion-induced increase of glutamate, but CPG did not inhibit. Administration of glutamine recovered the increased glutamate level in the MSO-treated rats. These results suggested that neurons, but not glial cells, play an important role in the heavy-ion-induced increase of glutamate.
