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. Author manuscript; available in PMC: 2014 Jul 1.
Published in final edited form as: Neurochem Int. 2013 Apr 23;63(1):42–46. doi: 10.1016/j.neuint.2013.04.006

Figure 1. Real-time FRET determinations of antiparkinsonian D2R agonist-mediated modulation of A2AR agonist binding.

Figure 1

(A) Chemical structures of the investigated antiparkinsonian D2R agonists (pramipexole, rotigotine and apomorphine). (B) Time-resolved changes in FRET signals engaged by MRS5424 (2 µM) in cells transfected with A2ARCFP and D2RAGT in the absence (black trace) or presence (red trace) of pramipexole (120 µM), rotigotine (1 µM) and apomorphine (6 µM) were recorded. Traces are representative of four separate experiments with similar qualitative and quantitative results. (C) The FRET increase (1/F480) was fitted by a simple monoexponential curve and the magnitude of the FRET signal (A, see experimental procedures) calculated for each experimental condition. Data represents the average ± S.E.M. values of four independent experiments. Asterisk indicates data significantly different from the control condition (i.e. in the absence of antiparkinsonian D2R agonist): *p < 0.01 by ANOVA with Dunnett`s multiple comparison post-hoc test.