Abstract
Amyloid β (Aβ) is the principal constituent of senile plaques in Alzheimer’s disease patients. We investigated whether Aβ and glutamate affect long-term potentiation (LTP) in rat hippocampal slices. Pretreatment with 1 μM Aβ1 – 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 μM glutamate alone for 3 h, pretreatment with Aβ1 – 42 and glutamate impaired LTP significantly. These results raise the possibility that neurotoxicity of Aβ is exacerbated by the enhancement of susceptibility to excitatory amino acids.
