Article Figures & Data
Figures
- Figure 1.
p-p38 MAPK at different times after one 5-min pulse of 5-HT (50 μM). A, Representative confocal images of p-p38 MAPK immunofluorescence in SNs immediately after the end of 5-HT. B, Representative confocal images of p-p38 MAPK immunofluorescence in SNs at 25 min after onset of 5-HT. C, Summary data. p-p38 MAPK levels were normalized to the mean of Veh controls. Treatment with 5-HT for 5 min significantly decreased p-p38 MAPK immediately after the end of treatment, whereas the same treatment led a significant increase in p-p38 MAPK when measured 25 min after onset of 5-HT. In this and other illustrations, data are presented by box-and-whisker plots. The median is indicated by the solid line in the interior of the box. The mean is indicated by the dashed line in the interior of the box. The lower end of the box is the first quartile (Q1). The upper end of the box is the third quartile (Q3). The ends of the vertical lines (whiskers) are the maximum and minimum values of nonoutliers. The small circles outside the whiskers are the outliers larger than Q3 + 1.5(Q3-Q1) or smaller than Q3-1.5(Q3-Q1). Scale bar, 20 μm. Significant differences are indicated by * for p < 0.05.
- Figure 2.
Biphasic regulation of p38 MAPK by one 5-min pulse of 5-HT (50 μM). A, Representative confocal images of p-p38 MAPK immunofluorescence in Aplysia SNs at different times after onset of 5-HT. Scale bar, 20 μm. B, Summary data. The percent change was calculated as the change of p-p38 MAPK level after 5-HT compared with control level. 5-HT induced a delayed increase in p-p38 MAPK, following a transient decrease immediately after treatment. p-p38 MAPK returned to the control level at 60 min. C, Statistical analysis revealed significant differences between Veh and 5-HT treatment groups at 5 and 45 min. p-p38 MAPK levels were normalized to the mean of Veh controls. Significant differences between the groups are indicated by * for p < 0.05.
- Figure 3.
The effect of p38 MAPK inhibitor on pERK. A, Representative confocal images of pERK immunofluorescence in SNs at 60 min after onset of a 5-min pulse of 5-HT, in the absence or presence of the p38 MAPK inhibitor SB203580 (SB). B, Summary data. Compared with the 5-HT alone group, treatment with 5-HT in the presence of SB induced a significant increase in pERK at 60 min after onset of 5-HT. Scale bar, 20 μm. Significant differences are indicated by * for p < 0.05.
- Figure 4.
The interaction between p38 MAPK and MAPKK/ERK pathways. A1, Representative confocal images of p-p38 MAPK immunofluorescence in SNs at 45 min after onset of 5-HT, in the absence or presence of the MEK1/2 inhibitor U0126. A2, Summary data. Treatment with U0126 induced a significant decrease in 5-HT induced p-p38 MAPK at 45 min. B1, Representative confocal images of p-p38 MAPK immunofluorescence in SNs at 60 min after onset of 5-HT, in the absence or presence of SB. B2, Summary data. No significant differences were found among the three groups. Scale bar, 20 μm. Significant differences are indicated by * for p < 0.05.
- Figure 5.
p-p38 MAPK 45-50 min after onset of different stimulus protocols. A, Representative confocal images of p-p38 MAPK immunofluorescence in SNs at 45-50 min after onset of 5-HT. B, Summary data. Levels of p-p38 MAPK was measured at 45 min after onset of a single 25-min 5-HT pulse, two 5-min duration pulses of 5-HT with ISI of 20 min, or one 5-min duration pulse of 5-HT. p-p38 MAPK was measured at 50 min after onset of two pulses of 5-HT with an ISI of 45 min. The last group produced less p-p38 MAPK than any of three former groups. Scale bar, 20 μm. Significant differences are indicated by * for p < 0.05.
- Figure 6.
Computational simulation of ERK and p38 MAPK phosphorylation after different 5-HT treatments. A, Schematic of the model of the ERK and p38 MAPK signaling pathways. Key pathways are labelled by numbers. B, Dynamics of pERK (B1) and p-p38 MAPK (B2) after one pulse of 5-HT. The simulations (black traces) are qualitatively similar to the empirical data (red circles) collected in the present study.
- Figure 7.
Computational simulation of the ratio of pERK to p-p38 MAPK after two or five pulses of 5-HT. A, Dynamics of pERK and p-p38 MAPK levels, and the ratio of pERK to p-p38 MAPK, for 2 hours after two pulses with ISI of 45 min (A1) or 60 min (A2). B, Dynamics of the ratio of pERK to p-p38 MAPK for two hours after five pulses with ISIs of the standard protocol (B1) or enhanced protocol (B2) as compared with the peak ratio of pERK to p-p38 MAPK after one pulse (∼1.2, dashed line).
Tables
Data structure Type of test Power a Non-normal distribution Wilcoxon signed-rank test 95% confidence interval of the difference: -20.6 to -1.2 b Non-normal distribution Wilcoxon signed-rank test 95% confidence interval of the difference: -4.6 to 35.2 c Non-normal distribution Wilcoxon signed-rank test 95% confidence interval of the difference: -16.7 to -0.4 d Normal distribution Paired t test Power: 0.956 e Normal distribution Paired t test Power: 0.992 f Normal distribution One-way RM ANOVA + Student--Newman--Keuls Power: 0.858 g Normal distribution One-way RM ANOVA + Student--Newman--Keuls Power: 0.805 h Normal distribution One-way ANOVA Power: 0.066 i Non-normal distribution Kruskal--Wallis one-way ANOVA on ranks + Student--Newman--Keuls Not applicable
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