Short communicationThe σ1 receptor agonist (+)-pentazocine increases store-operated Ca2+ entry in MCF7σ1 and SK-N-SH cell lines

BackgroundThe intracellular [Ca2+] is modulated by σ receptors. An important component of the cellular machinery governing the intracellular [Ca2+] is Store-Operated Calcium Entry (SOCE). Here we want to investigate whether ligands of σ receptors affect SOCE.MethodsThe intracellular [Ca2+] was monitored, with the fluorescent Ca2+-sensitive probe Fura-2, in four cell lines with a different expression of σ receptors, namely MCF7 (expressing σ1 receptors with a low density and overexpressing σ2 receptors), MCF7σ1 (overexpressing σ1 receptors), SK-N-SH, and HT-29.ResultsWhen thapsigargin was used to deplete intracellular Ca2+ stores, in a Ca2+-free incubation medium, the Ca2+ influx (following Ca2+ re-addition) was significantly increased by 1 μM (+)-pentazocine (σ1 receptor agonist) in MCF7σ1 (by 22.5%) and SK-N-SH (by 45.6%), but not in HT-29 and MCF7 cells. We have used, as a second approach, the “Mn2+ quenching” protocol. In MCF7σ1 cells, after thapsigargin treatment, the fluorescence quenching induced by Mn2+ influx (evidence of Ca2+ influx) was significantly increased (by 25.8%) by 1 μM (+)-pentazocine, significantly decreased (by 18.0%) by BD1063 (σ1 receptor antagonist), and not affected by the presence of both ligands. These effects were not observed in MCF7 cells. Finally, in MCF7 cells, 1 μM PB28 (σ2 receptor agonist), did not affect both the Ca2+ response after Ca2+ re-addition and the fluorescence quenching induced by Mn2+ influx.ConclusionsWe propose that the σ1 receptor agonist (+)-pentazocine increases SOCE in MCF7σ1 and SK-N-SH cell lines. The σ2 receptor agonist PB28 does not affect SOCE in MCF7 cells.