Open AccessClostridium perfringens epsilon toxin causes excessive release of glutamate in the mouse hippocampus
Author(s) -
Miyamoto Osamu,
Sumitani Kazunori,
Nakamura Takehiro,
Yamagami Shinichi,
Miyata Shigeru,
Itano Toshifumi,
Negi Tetsuro,
Okabe Akinobu
Publication year - 2000
Publication title -
fems microbiology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.899
H-Index - 151
eISSN - 1574-6968
pISSN - 0378-1097
DOI - 10.1111/j.1574-6968.2000.tb09215.x
Subject(s) - glutamate receptor , microdialysis , toxin , riluzole , hippocampal formation , clostridium perfringens , hippocampus , neurotoxicity , chemistry , pharmacology , neurotoxin , efflux , tetrodotoxin , biology , biochemistry , neuroscience , extracellular , biophysics , toxicity , bacteria , receptor , genetics , organic chemistry
The mechanism of neurotoxicity of Clostridium perfringens epsilon toxin to the mouse brain was investigated. Intravenous injection in mice with the toxin caused seizure and excited hippocampal neurons. Microdialysis revealed that epsilon toxin induced excessive glutamate release in the hippocampus. Both the seizure and glutamate release were attenuated by prior injection with riluzole, an inhibitor of pre‐synaptic glutamate release, suggesting that this toxin enhances glutamate efflux, leading to seizure and hippocampal neuronal damage.