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. Author manuscript; available in PMC: 2015 Feb 23.
Published in final edited form as: J Neurophysiol. 2002 Oct;88(4):1851–1858. doi: 10.1152/jn.2002.88.4.1851

FIG. 2.

FIG. 2

Systems level effects of Nic and Antag. A: Nic (0.5 μM) increased respiratory frequency; this effect slightly desensitized. Nic was bath applied at time 0 min and was continuously present for 30 min (n = 3). B: the effects of nicotinic antagonists α-BgTx (n = 4) or MLA (n = 6) on Nic-induced increase in respiratory frequency are not significant compared with control (Ctrl). DH-β-E (n = 4), HMT (n = 5) and d-TC (n = 6) reversed these effects. Control value was taken at about 10 min during bath application of nicotine in the group of control experiment as A without adding antagonist. Ten minutes was equivalent to the time the effects of antagonists were measured (4–6 min after Antag application and Antag was applied 3–5 min after Nic application) in the groups of antagonist experiments. Two-way repeated-measures ANOVA and the post hoc analysis based on Dunnett were used to analyze the change in frequency with antagonists compared with the control desensitization. C: the effects of α-BgTx or MLA on nicotine-induced decrease in amplitude of inspiratory bursts were not significant, while DH-β-E, HMT and d-TC reversed these nicotinic effects. One-way repeated-measures ANOVA for each group and post hoc analysis based on Tukey (SAS Institute 1999) were used. *, statistically significant. The frequency and amplitude data were normalized to baseline values prior to Nic application for each preparation. Raw data (nonnormalized) were used in statistical tests.