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. Author manuscript; available in PMC: 2011 Nov 18.
Published in final edited form as: Vis Neurosci. 2009 Jun 5;26(3):267–274. doi: 10.1017/S0952523809090105

Fig. 5.

Fig. 5

Effects of β-ionone on rod and cone cyclic nucleotide-gated channels. Current–voltage relationships for homomeric rod (n = 3) (A) and cone cyclic nucleotide-gated channels (n = 1) (B). Xenopus oocytes expressing bovine rod (A) or human cone (B) homomeric channels. Voltage was stepped to ±100 mVin 50-mVincrements from a holding potential of 0 mV. Currents were normalized by the value obtained in saturating cGMP without β-ionone. ○, 2 mM cGMP; △, 2 mM cGMP + 10 μM β-ionone; ▽, 2 mM cGMP + 20 μM β-ionone. Error bars in (A and B) demarcate SEM. Low concentrations of β-ionone had little or no effect on the channels. Currents elicited through native cyclic nucleotide-gated channels from patches excised from tiger salamander GS rod outer segments in the presence of saturating cGMP without (C) or with 115 μM β-ionone (D). Current decreased when the patch was placed in concentrated β-ionone. Leak currents in the absence of cGMP were subtracted from all recordings. SEM, standard error of mean.