FIGURE 6.
The counteractive effect of 5-HT2A/C on 5-HT1A regulation of NMDAR function is dependent on the β-arrestin/ERK pathway. A, top: Western blots of β-arrestin 1/2 in PFC cultures transfected without or with siRNA against β-arrestin 1/2 or a scrambled siRNA. Quantification of β-arrestin 1/2 expression under different conditions. Each point represents mean ± S.E. of three independent experiments. *, p < 0.001, ANOVA. B, top: Western blots of phospho-ERK in the absence or presence of α-Me-5HT (20 μm, 3 min) in PFC cultures transfected with or without β-arrestin 1/2 siRNA. Bottom: quantification of phospho-ERK under different conditions. Each point represents mean ± S.E. of 4–5 independent experiments. *, p < 0.001, ANOVA. C, plot of peak NMDAR currents as a function of time and 8-OH-DPAT (20μm) application in the presence ofα-Me-5HT (20 μm) in GFP-positive neurons transfected with or without siRNA against β-arrestin 1/2. D, cumulative data (mean ± S.E.) summarizing the percentage reduction of NMDAR currents by 8-OH-DPAT in the absence or presence ofα-Me-5HT under different conditions. *, p < 0.001, ANOVA.