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. 2013 Jul 26;2(9):941–951. doi: 10.1242/bio.20135215

Fig. 5. Pharmacological study of the transient voltage-dependent K+ current in LNCaP-NE cells (A,B,C) and LNCaP-α1H cells (D).

Fig. 5.

(A) On-line recording of transient voltage-dependent K+ currents inhibition by NiCl2 (10 µM) and TEA-Cl (20 mM). Inset: representative membrane currents measured at −20 mV from HP −80 mV. (B) Inhibition of membrane currents (measured at −20 mV from HP −80 mV) by TEA (20 mM) and iberiotoxin (Iberio, 1 µM), but not by apamin (Apa, 500 nM). (C) Inhibition of voltage-dependent K+ current by si-hBK (20 nM). i–v curves shown here represent the average difference between currents obtained at HP −80 mV and those obtained at HP −40 mV. Inset: representative membrane currents measured at −20 mV from HP −80 mV. (D) Representative inhibition of membrane currents (measured at −20 mV from HP −80 mV) by si-hBK (20 nM) and si-α1H1 and si-α1H2 (5 nM), but not by si-Ctl (20 nM) or si-hIK1 (20 nM). Treatments for 3 days with si-hBK (20 nM) inhibit about 80% of the Ca2+-dependent K+ current in both LNCaP-NE (C) and LNCaP-α1H (D) cells.