Amyloid-b and Alzheimer's disease type pathology differentially affects the calcium signalling toolkit in astrocytes from different brain regions

A. A. Grolla, J. A. Sim, D. Lim, J. J. Rodriguez, A. A. Genazzani, A. Verkhratsky

    Research output: Contribution to journalArticlepeer-review

    Abstract

    The entorhinal'hippocampal circuit is severely affected in Alzheimer's disease (AD). Here, we demonstrate that amyloid-β (Aβ) differentially affects primary cultured astrocytes derived from the entorhinal cortex (EC) and from the hippocampus from nontransgenic controls and 3xTg-AD transgenic mice. Exposure to 100 nM of Aβ resulted in increased expression of the metabotropic glutamate receptor type 5 (mGluR5) and its downstream InsP 3 receptor type 1 (InsP3R1) in hippocampal but not in EC astrocytes. Amplitudes of Ca2+ responses to an mGluR5 agonist, DHPG, and to ATP, another metabotropic agonist coupled to InsP3Rs, were significantly increased in Aβ-treated hippocampal but not in EC astrocytes. Previously we demonstrated that senile plaque formation in 3xTg-AD mice triggers astrogliosis in hippocampal but not in EC astrocytes. The different sensitivities of the Ca2+ signalling toolkit of EC versus hippocampal astrocytes to Aβ may account for the lack of astrogliosis in the EC, which in turn can explain the higher vulnerability of this region to AD. © 2013 Macmillan Publishers Limited. All rights reserved.
    Original languageEnglish
    Article numbere623
    JournalCell Death and Disease
    Volume4
    Issue number5
    DOIs
    Publication statusPublished - May 2013

    Keywords

    • Alzheimer's disease
    • Amyloid-β
    • Astrocytes
    • Calcium deregulation
    • Entorhinal cortex
    • Hippocampus

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