Glutamate exacerbates amyloid beta1-42-induced impairment of long-term potentiation in rat hippocampal slices.
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.
Nakagami
Yasuhiro
Y
Neuroscience and Immunology Research Laboratories, Sankyo Co., Ltd., Tokyo, Japan. yasuhiro@shina.sankyo.co.jp
Oda
Tomiichiro
T
D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D000818:Animals; D004347:Drug Interactions; D018698:Glutamic Acid / Q000494:pharmacology*; D006624:Hippocampus / Q000187:drug effects* / Q000503:physiopathology; D017774:Long-Term Potentiation / Q000187:drug effects*; D008297:Male; D009498:Neurotoxins / Q000494:pharmacology; D010446:Peptide Fragments / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
D016229:Amyloid beta-Peptides; D009498:Neurotoxins; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D018698:Glutamic Acid