The knockdown of TASK-1 channels improved the proliferation of N2A cells.

Previous studies indicated that K(+) channels, such as voltage-gated Kv channels, were involved in the apoptosis and proliferation of neurons. In the experiments here, the small interfering RNAs (siRNAs) targeted against TASK-1, an acid-sensitive member of two-pore domain K(+) (K2P) channel family, were transfected into mouse neuroblastoma N2A cells. This treatment induced a reduction of messenger RNA (mRNA) level of TASK-1 by 61%. As a negative control, however, the transfection of scrambled siRNAs (scRNA) did not significantly affect the expression of TASK-1 in N2A cells. Furthermore, exposure to TASK-1-specific siRNAs (siTASK-1) for 48 h also substantially increased the proliferation rates of N2A cells by 25.8%, but no effect was observed in scRNA-treated cells. These data implied that TASK-1 channels may participate in the regulation of neuronal proliferation.