Hippocampal alterations in glutamatergic signaling during amyloid progression in AβPP/PS1 mice.

ABSTRACT: Our previous research demonstrated that soluble amyloid-β (Aβ)₄₂, elicits presynaptic glutamate release. We hypothesized that accumulation and deposition of Aβ altered glutamatergic neurotransmission in a temporally and spatially dependent manner. To test this hypothesis, a glutamate selective microelectrode array (MEA) was used to monitor dentate (DG), CA3, and CA1 hippocampal extracellular glutamate levels in 2-4, 6-8, and 18-20 month-old male AβPP/PS1 and age-matched C57BL/6J control mice. Starting at 6 months of age, AβPP/PS1 basal glutamate levels are elevated in all three hippocampal subregions that becomes more pronounced at the oldest age group. Evoked glutamate release was elevated in all three age groups in the DG, but temporally delayed to 18-20 months in the CA3 of A

SUBMITTER: Hascup KN 

PROVIDER: S-EPMC7467928 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature