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. Author manuscript; available in PMC: 2016 Oct 21.
Published in final edited form as: Cell Rep. 2016 Jul 21;16(6):1518–1526. doi: 10.1016/j.celrep.2016.06.098

Fig 4. D3R-dependent regulation of CaV3.2 currents in HEK 293 cells.

Fig 4

A) CaV3.2 steady-state activation and inactivation in HEK293 cells co-expressing D3R. Data are from untreated cells.

B) Peak activation current for CCh+quinpirole and CCh+quinpirole+sulpiride conditions. Data are fit to a Boltzmann equation. n = 8 each. Bars are SEM.

C) Activation and inactivation curves for CCh+quinpirole and CCh+quinpirole+sulpiride conditions. Activation: n = 8 each. Inactivation: n = 11 CCh+quinpirole, n = 9 CCh+quinpirole+sulpiride. Bars are SEM.

D) Half inactivation voltage is hyperpolarized by co-application of CCh and quinpirole. A concentration of ryanodine (5 μM) that activates RyR-dependent stores is ineffective in HEK cells. CCh+Quin effects are blocked by inhibiting D3R signaling with sulpiride, blocking ERK1/2 signaling with U0126, or preventing Gβγ-dependent recruitment of β-arrestin to D3R with pertussis toxin. Circles are single cells. Bars are mean ± SEM. **, p < 0.01, ANOVA, Newman-Keuls.

E) Half-activation voltage is hyperpolarized by co-application of CCh and quinpirole vs carbachol alone, but not quinpirole or quinpirole/CCh/sulpiride. Dots are single cells. Bars are mean ± SEM. *, p < 0.05, ANOVA, Newman-Keuls.