Indirect evidence supports altered glutamate signaling with Alzheimer's disease, however, it is not known if glutamate neurotransmission is impacted prior to cognitive decline. We examined cognition and glutamate neurotransmission in 2-4 month AβPP/PS1, an Alzheimer's disease model, and age-matched control mice. There were no differences in learning and memory as assessed by Morris water maze. However, in vivo electrochemical measures of potassium-evoked glutamate release in the CA1, but not the CA3 or dentate, was significantly elevated in AβPP/PS1 mice. These data support changes in the glutamatergic system that precedes cognitive decline in a mouse model of Alzheimer's disease.



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