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. Author manuscript; available in PMC: 2016 Apr 8.
Published in final edited form as: J Neurochem. 2013 Jul 30;127(1):57–65. doi: 10.1111/jnc.12359

Fig. 2.

Fig. 2

Residues 212–215 of D2 like dopamine receptor (D2R) are required for arrestin-mediated uncoupling of D2R responses in Xenopus oocytes. (a) Representative current traces of Kir3 responses elicited via dopamine activation of D2R (top) and the D2R212–215(IYIV)→A mutant (bottom). Control oocytes were injected with cRNA for the Kir3 subunits, Kir3.1 and Kir3.2, and either D2R or the D2R212–215(IYIV)→A mutant. Some oocytes in each of the groups injected with either D2R or D2R212–215(IYIV)→A cRNA were also injected with cRNA for β-arrestin2 (ARRB2) as indicated. The traces represent the baseline subtracted Kir3 responses elicited after perfusion of oocytes with dopamine (1 μM, bottom row). Vertical line marks on the traces indicate the time at which dopamine was washed out. (b) Quantification of the desensitization rates of D2R and the D2R212–215(IYIV)→A-activated Kir3 responses in control oocytes (white bar) or in oocytes injected with cRNA for ARRB2 (black bar, mean ± SEM, n = 4). ARRB2 co-expression significantly increased the desensitization rate of D2R responses (p < 0.0005, t-test) but not of D2R212–215(IYIV)→A. (c) Dopamine dose-response curves for D2R and D2R212–215(IYIV)→A-mediated Kir3 activation. The response at each dose is expressed as a percent of the average maximal response (n = 4). The EC50 (nM) derived for the dopamine-mediated activation of D2R and D2R212–215(IYIV)→A was 70.7 ± 10.6 and 99.4 ± 38.3 nM (mean ± SD), respectively, and were not significantly different between the two receptors.