Astrocytes respond to a neurotoxic Aβ fragment with state-dependent Ca²⁺ alteration and multiphasic transmitter release.

ABSTRACT: Excessive amounts of amyloid β (Aβ) peptide have been suggested to dysregulate synaptic transmission in Alzheimer's disease (AD). As a major type of glial cell in the mammalian brain, astrocytes regulate neuronal function and undergo activity alterations upon Aβ exposure. Yet the mechanistic steps underlying astrocytic responses to Aβ peptide remain to be elucidated. Here by fluorescence imaging of signaling pathways, we dissected astrocytic responses to Aβ25-35 peptide, a neurotoxic Aβ fragment present in AD patients. In native health astrocytes, Aβ25-35 evoked Ca²⁺ elevations via purinergic receptors, being also dependent on the opening of connexin (CX) hemichannels. Aβ25-35, however, induced a Ca²⁺ diminution in Aβ-preconditioned astrocytes as a result of the poten

SUBMITTER: Pham C 

PROVIDER: S-EPMC7968286 | biostudies-literature | 2021 Mar

REPOSITORIES: biostudies-literature