Abstract
Human amyloid-β1-40 (Aβ1-40) and rat Aβ1-42 have lower affinity for extracellular Zn2+ than human Aβ1-42. Here we report extracellular Zn2+-independent attenuation of dentate gyrus long-term potentiation (LTP) by human Aβ1-40 and rat Aβ1-42. On the basis of the data that dentate gyrus LTP is extracellular Zn2+-dependently attenuated after local injection of human Aβ1-42 (25 pmol, 1 μl) into the dentate gyrus, which increases intracellular Zn2+ in the dentate gyrus, the toxicity of human Aβ1-40 and rat Aβ1-42 was compared in the in vivo system with human Aβ1-42. Dentate gyrus LTP was attenuated after injection of human Aβ1-40 and rat Aβ1-42 (25 pmol, 1 μl) into the dentate gyrus, which did not increase intracellular Zn2+ in the dentate gyrus. The attenuated LTP was not rescued by co-injection of CaEDTA, an extracellular Zn2+ chelator. The present study suggests that human Aβ1-40 and rat Aβ1-42 affect cognitive activity via extracellular Zn2+-independent mechanism at low micromolar concentration.
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