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. 2002 Jul 1;22(13):5310–5320. doi: 10.1523/JNEUROSCI.22-13-05310.2002

Fig. 8.

Fig. 8.

PACAP rapidly phosphorylates ERK, increases cAMP, and elevates VIP mRNA. A, PACAP (100 nm) phosphorylates ERK1/2. The ability of PACAP to phosphorylate ERK1/2 continues for up to 6 hr of PACAP exposure. By 24 hr, PACAP stimulatory effects are gone. Upregulation of phospho-ERK by PACAP (P) is completely inhibited by 30 μm U0126 (U) at all time points, whereas total ERK levels are unaffected. C, Control-treated cells. B, PACAP elevates cAMP for 6 hr. Cells were treated as described in Materials and Methods and harvested for cAMP measurements at 0 min, 30 min, and 6 hr with or without 100 nm PACAP. C, PACAP stimulation of VIP at 6 hr is blocked by U0126. Cells were treated with the MEK inhibitor 30 μm U0126 (U01) or vehicle (0.1% ethanol in culture medium) 30 min before and during exposure to 100 nm PACAP and harvested for RNA and Q RT-PCR as described in Figure7A. Values are the mean ± SEM of three separate wells from a single chromaffin cell dispersion. Values represent uncorrected data demonstrating specificity of U0126 for VIP blockade compared with ENK and GAPDH.