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Circadian and Social Cues Regulate Ion Channel Trafficking

Figure 9

Disrupting vesicular trafficking prevents the ACTH-induced increase in the inward rectifier potassium current (IKIR) but has no effect on the delayed rectifier current (IKDR).

(A,B) CQ and NEM prevented the ACTH-induced increase in IKIR magnitude. I-V curves depict normalized steady-state IK at baseline and after 30 min exposure to CQ or NEM, then 30 minutes after addition of ACTH. Potassium currents are isolated in all conditions by blocking INa with 1 ┬ÁM TTX. The apparent increase in DR current with NEM treatment plus ACTH is not statistically significant when compared at individual membrane voltages. Insets: summary of peak IKIR at baseline and after 30 min exposure to CQ or NEM, then 30 min after addition of ACTH. Both compounds produced a decrease in current magnitude. Asterisks indicate conditions significantly different from baseline by Tukey's HSD following significant omnibus repeated measures ANOVA (for CQ F[2,4,8] = 26.6, p<0.001; NEM F[2,5,10] = 6.00, p<0.05). (C) The magnitude of IKDR at peak current is not changed by CQ or CQ with ACTH (F[2,4,8] = 2.76, p>0.1). (D) The magnitude of IKDR at peak current was not changed in the presence of NEM or NEM with ACTH (F[2,5,10] = 0.12, p>0.8).

Figure 9

doi: https://doi.org/10.1371/journal.pbio.1000203.g009