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 neurons (iSyn mice), mice expressing human wildtype α-synuclein (I2-2 mice), and mice expressing A30P mutant α-synuclein (O2 mice). This evidence concerns the gene SNCA and synucleinopathy.