Dysregulation of astrocytic Ca²⁺ signaling and gliotransmitter release in mouse models of α-synucleinopathies.

ABSTRACT: α-Synuclein is a major component of Lewy bodies (LB) and Lewy neurites (LN) appearing in the postmortem brain of Parkinson's disease (PD) and other α-synucleinopathies. While most studies of α-synucleinopathies have focused on neuronal and synaptic alterations as well as dysfunctions of the astrocytic homeostatic roles, whether the bidirectional astrocyte-neuronal communication is affected in these diseases remains unknown. We have investigated whether the astrocyte Ca²⁺ excitability and the glutamatergic gliotransmission underlying astrocyte-neuronal signaling are altered in several transgenic mouse models related to α-synucleinopathies, i.e., mice expressing high and low levels of the human A53T mutant α-synuclein (G2-3 and H5 mice, respectively) globally or selectively in neu

SUBMITTER: Nanclares C 

PROVIDER: S-EPMC10119048 | biostudies-literature | 2023 May

REPOSITORIES: biostudies-literature