@article{oai:fukuyama-u.repo.nii.ac.jp:00006930,
 author = {田村, 豊 and 塩見, 浩人},
 journal = {福山大学薬学部研究年報, Annual report of the Faculty of Pharmacy & Pharmaceutical Sciences, Fukuyama University},
 month = {},
 note = {P(論文), Glutamate is well known as an excitatory neurotransmitter in the vertebrate central nervous system (CNS). Recently, glutamate is also postulated to play an important role in the pathogenesis of the neuronal cell loss that is associated with several neurological disease states in the CNS. Glutamate neurotoxicity in the cultured cortical neurons is mediated by nitric oxide(NO). As the excitatory action of glutamate is regulated by other neurotransmitters, the neurotoxic action of glutamate may be affected by other endogenous substances. We have previously found that cholecystokinin(CCK) prevented glutamate neurotoxicity in the cultured cortical neurons. The evidence has suggested that CCKB receptor stimulation causes suppression of a step in NO formation triggered by N-methyl-D-aspartate(NMDA) receptor activation. CCK may have a role to promote cell survival in the life-regulatory function of the CNS. This review mainly discusses the mechanisms of glutamate neurotoxicity and CCK-induced protection against glutamate neurotoxicity.},
 pages = {16--37},
 title = {グルタミン酸神経毒性と内因性神経保護物質},
 volume = {13},
 year = {1995}
}