Open AccessGlutamate Exacerbates Amyloid β1 − 42-Induced Impairment of Long-Term Potentiation in Rat Hippocampal Slices
Author(s) -
Yasuhiro Nakagami,
Tomiichiro Oda
Publication year - 2002
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.88.223
Subject(s) - long term potentiation , hippocampal formation , neuroscience , glutamate receptor , term (time) , hippocampus , long term depression , amyloid (mycology) , chemistry , psychology , ampa receptor , physics , biochemistry , inorganic chemistry , quantum mechanics , receptor
Amyloid beta (A beta) is the principal constituent of senile plaques in Alzheimer's disease patients. We investigated whether A beta and glutamate affect long-term potentiation (LTP) in rat hippocampal slices. Pretreatment with 1 microM A beta1-42 alone for 3 h slightly inhibited LTP; however, the potentiation was maintained for 60 min. Although the impairment was not observed by pretreatment with 30 microM glutamate alone for 3 h, pretreatment with A beta1-42 and glutamate impaired LTP significantly. These results raise the possibility that neurotoxicity of A beta is exacerbated by the enhancement of susceptibility to excitatory amino acids.