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. 2012 Feb 22;32(8):2683–2695. doi: 10.1523/JNEUROSCI.4125-11.2011

Figure 4.

Figure 4.

Neurabin attenuates A1R-mediated responses in vivo. A, Neurabin-deficient mice are more sensitive to R-PIA-elicited sedation, as assessed by rotarod latency. The EC50 values for sedation in Nrb−/− (n = 8) and corresponding WT littermates (n = 5) are 1.29 and 2.64 mg/kg, respectively. *p < 0.05; **p < 0.01. B, The α2AR-agonist, UK14,304, induces comparable sedation responses in both WT and Nrb−/− mice as assessed by rotarod latency. n = 5 for both WT and Nrb−/− mice. Error bars indicate mean ± SEM. C, The density of A1Rs is indistinguishable in brain membrane preparations obtained from WT and Nrb−/− mice as measured by saturation binding assays. Values represent mean ± SEM; n = 3 for each genotype. The Bmax values predicted by nonlinear regression fit for the A1R in WT and Nrb−/− brain homogenates are 1547 ± 90 and 1515 ± 76 fmol/mg protein, respectively. D, The intrinsic affinity of the A1R for R-PIA in brains of WT mice is similar to that in brains of Nrb−/− mice. Competition binding assays were performed in the presence of 100 μm Gpp(NH)p. Binding of the [3H]DPCPX radioligand is given as a percentage of binding without competitors. Values represent mean ± SEM; n = 3 for each genotype. The IC50 values predicted for R-PIA in competition for radioligand binding in WT and Nrb−/− brain homogenates are 0.41 ± 0.11 and 0.29 ± 0.12 μm, respectively.