Abstract
In the present study, the ability of muscarinic cholinergic receptors (mAChRs) to regulate the uptake of glutamate (monitored as D‐aspartate) into human SH‐SY5Y neuroblastoma cells under isotonic or hypotonic conditions has been examined. In isotonic media, agonist activation of mAChRs resulted in a significant increase (250–300% of control) in the uptake of D‐aspartate and concurrently, a cellular redistribution of the excitatory amino acid transporter 3 (EAAT3) to the plasma membrane. In hypotonic media, the ability of mAChR activation to facilitate D‐aspartate uptake was significantly attenuated (40–50%) and the cellular distribution of EAAT3 was disrupted. Reduction of mAChR‐stimulated D‐aspartate uptake under hyposmotic conditions could be fully reversed upon re‐exposure of the cells to isotonic media. Under both isotonic and hypotonic conditions, mAChR‐mediated increases in D‐aspartate uptake were dependent upon cytoskeletal integrity, protein kinase C (PKC) and phosphatidylinositol 3‐kinase (PI3K) activities and the availability of intracellular Ca2+. In contrast, a dependence on extracellular Ca2+ was only observed under isotonic conditions. The results suggest that although the uptake of D‐aspartate into SH‐SY5Y cells is enhanced following mAChR activation, this process is markedly attenuated by hyposmolarity. Supported by GM007767 (DJF).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.