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. 2009 Jun 3;29(22):7137–7147. doi: 10.1523/JNEUROSCI.0544-09.2009

Figure 1.

Figure 1.

K+ channel expression in AMCs derived from P0 pups born to saline-treated versus nicotine-treated dams. In A1–A3, mean (±SEM) current density versus voltage plots are shown for saline-treated AMCs exposed to control (C) and either the BK channel blocker IbTx (100 nm; n = 10) (A1), the SK channel blocker Apa (100 nm; n = 10) (A2), or the nonspecific blocker of Ca2+ channels cadmium (Cd2+) (50 μm; n = 10) (A3), which indirectly blocks Ca2+-dependent K+ channels. The insets show sample recordings at +30 mV; holding potential was −60 mV. Corresponding data for P0 nicotine-treated AMCs are shown in B1–B3 (n = 10). Note nicotine-treated AMCs expressed similar Ca2+-dependent K+ currents as saline-treated AMCs. Isolated AMCs from pups exposed to nicotine in utero also showed expression of the K+ channel subunits Kv1.2 and Kv1.5, BK (α-subunit), and SK2, as determined by immunofluorescence (C).