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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Neuropharmacology. 2015 Oct 9;101:291–308. doi: 10.1016/j.neuropharm.2015.10.006

Figure 11.

Figure 11

The PACAP38-mediated reduction in Kv4.2 currents is attenuated in channels with phospho-disruptive mutations at ERK1/2-phosphorylation sites. Representative traces of whole-cell voltage-clamp recordings (using similar voltage protocol as in Fig. 8) from HEK293T cells transfected with plasmids containing Kv4.2-T602A (A) or Kv4.2-T607A (B) or Kv4.2-S616A (C) or Kv4.2-T602A/T607A/S616A triple mutant (D) cDNAs, along with the plasmids containing KChlP2 and PAC1-Null cDNAs. Current density – voltage plots for these mutant channels, without or with PACAP38 treatment (100 nM, 20 min) are given next to the current traces under each panel. Data are presented as mean ± SEM (n = 5-7 cells for A, 7 cells for B, 10-11 cells for C, and 7-9 cells for D). * denotes p<0.05, significantly different for PACAP38 treatment conditions compared to current densities at respective voltage pulses under control conditions (Unpaired Student's t-test).