Abstract
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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