Fig. 2.

Involvement of IP₃R1, but not IP₃R3 in haloperidol-induced changes in levels of cytosolic calcium and translocation of the IP₃R1 and σ1R to the nucleus following haloperidol treatment. Experiments were performed on NG-108 cells differentiated by dbcAMP. To determined haloperidol-induced changes in cytosolic calcium due to IP₃R1/IP₃R3 receptors, these receptors were silenced either individually, or both of them and levels of cytosolic calcium levels were determined after haloperidol treatment (a). Silencing of IP₃R1, but not IP₃R3 caused significant decrease in cytosolic calcium levels, thus proving involvement of the IP₃R1, but not IP₃R3 in haloperidol-induced increase in cytosolic calcium. In control cells (cont), IP₃R1s (b, green signal) and σ1Rs (c, green signal) are localized to the ER. Following haloperidol treatment (Hμ; 10 µmol/L), these receptors translocate to the nucleus (b, c, green signal). Translocation of the IP₃R1 and σ1R was verified by z-stacks from the Hμ-treated cells (d), which clearly shows an intranuclear signal. In the presence of Xestospongin C (Xest; 1 µmol/L), the Hμ -induced translocation of σ1R does not occur (e, HμXest). Results in the graph are expressed as the mean ± SEM and represent an average of six parallels from two independent cultivations. Statistical significance compared to control was ***p < 0.0001 and compared to Hμ treated cells was +++p < 0.0001