ALS-Associated SOD1(G93A) Decreases SERCA Pump Levels and Increases Store-Operated Ca²⁺ Entry in Primary Spinal Cord Astrocytes from a Transgenic Mouse Model.

ABSTRACT: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by the selective death of motor neurons (MNs), probably by a combination of cell- and non-cell-autonomous processes. The past decades have brought many important insights into the role of astrocytes in nervous system function and disease, including the implication in ALS pathogenesis possibly through the impairment of Ca²⁺-dependent astrocyte-MN cross-talk. In this respect, it has been recently proposed that altered astrocytic store-operated Ca²⁺ entry (SOCE) may underlie aberrant gliotransmitter release and astrocyte-mediated neurotoxicity in ALS. These observations prompted us to a thorough investigation of SOCE in primary astrocytes from the spinal cord of the SOD1(G93A) ALS mou

SUBMITTER: Norante RP 

PROVIDER: S-EPMC6829245 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature