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. 2008 Dec 18;41(1):93–99. doi: 10.1165/rcmb.2008-0352OC

Figure 5.

Figure 5.

Effect of the α7 nAChR antagonist, MLA, on increases in nicotine-induced current caused by genistein. (A, a) Inward current induced by 50 μM nicotine in a control cell (note: same tracing as used in Figure 4A, a). (A, b) MLA (20 nM) inhibited the genistein-enhanced nicotine currents by approximately 66%, with a slower desensitizing current remaining. (A, c) Mec (25 μM) inhibited all the genistein-enhanced nicotine currents. (B) Genistein significantly increased the MLA-sensitive component of nicotine-induced inward current. The MLA-sensitive component of nicotine-induced (50 μM) inward current was 65.2 (±6) pA (n = 4). Genistein (30 μM) increased the MLA-sensitive component of nicotine-induced inward current to 152.1 (±34) pA (n = 4), a 2.3-fold increase. Open bars, MLA; solid bars, MLA + Genistein. Numbers in parentheses indicate the number of cells averaged (mean ± SEM; *P < 0.05).