Stimulation of EAAC1 in C6 glioma cells by store-operated calcium influx

Biochimica Et Biophysica Acta
Andrew MurphyGethin J McBean

Abstract

This study investigated how modulation of intracellular calcium alters the functional activity of the EAAC1 glutamate transporter in C6 glioma cells. Pre-incubation of C6 glioma cells with the endoplasmic reticulum Ca2+ ATP pump inhibitor, thapsigargin (10 microM) produced a time-dependent increase in the Vmax for D-[3H]aspartate transport that reached a maximum at 15 min (143% of control; P<0.001) that was accompanied by increased plasma membrane expression of EAAC1 and was blocked by inhibition of protein kinase C. Pre-incubation of C6 glioma cells with phorbol myristate-3-acetate (100 nM for 20 min) also caused a significant increase in the Vmax of sodium-dependent D-[3H]aspartate transport (190% of control; P<0.01). In contrast, in the absence of extracellular calcium, thapsigargin caused a significant inhibition in D-[3H]aspartate transport that was not mediated by protein kinase C. Blockade of store-operated calcium channels with 2-aminoethoxydiphenyl borate (50 microM) or SKF 96365 (10 microM) caused a net inhibition of D-[3H]aspartate uptake. Co-incubation of C6 glioma cells with both thapsigargin and 2-aminoethoxydiphenyl borate (but not SKF 96365) prevented the increase in D-[3H]aspartate transport that was observed i...Continue Reading

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Citations

Jan 19, 2010·The Journal of Pharmacology and Experimental Therapeutics·Daniel J FosterStephen K Fisher
Sep 28, 2010·Cytometry. Part a : the Journal of the International Society for Analytical Cytology·Alice VinesAlfonso Blanco-Fernández
Apr 13, 2011·Journal of Biomechanics·Geraldine M KellySuzanne P Jarvis
Nov 26, 2010·Metabolic Brain Disease·Zafeer Baber, Nasrin Haghighat
Apr 25, 2021·Neurochemical Research·Alain M GuillemMichael B Robinson

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