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Circadian and Social Cues Regulate Ion Channel Trafficking

Figure 6

ACTH increases the inward rectifier potassium current (IKIR) via a cAMP/PKA pathway; the delayed rectifier current (IKDR) is stable across all conditions.

(A) Representative family of electrocyte potassium currents recorded with INa blocked by 1 ┬ÁM TTX. To generate the IV curves in Panel B, current amplitude was measured at steady state (open square in A). (B) Normalized IV curves at baseline and after 20 min exposure to saline (control) or ACTH. (C) Both ACTH and the cAMP analog 8-Br-cAMP increase the magnitude of IKIR. The PKA blocker H89 had no effect alone, but pretreatment with H89 blocked the ACTH- and 8-Br-cAMP-induced increase in IKIR magnitude. Asterisks indicate conditions different from saline controls (ANOVA F[5, 34] = 16.22, p<0.0001; pairwise comparisons by Tukey's HSD). (D) The delayed rectifier was stable across all experimental conditions (ANOVA F[5, 34] <1, p>0.5).

Figure 6