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. Author manuscript; available in PMC: 2009 Dec 22.
Published in final edited form as: J Pharmacol Exp Ther. 2007 Nov 21;324(2):484–496. doi: 10.1124/jpet.107.129890

Fig. 7.

Fig. 7

2,4-Epi-neoDH is a KAR antagonist. A, representative traces of glutamate-evoked currents (10 mM) from GluR5-2a and GluR6a receptors before application of 30 μM 2,4-epi-neoDH; subsequent glutamate-evoked currents in the presence of the analog were attenuated. B, currents from GluR4(i) receptors were not reduced by 300 μM 2,4-epi-neoDH. C, inhibition-response curves for 2,4-epi-neoDH on recombinant GluR4(i), GluR5-2a, and GluR6a receptors. Logistic fits were constrained to fixed minima (0%) and maxima (100%), and IC50 values were determined to be 7.5 and 74 μM for GluR5-2a and GluR6a receptors, respectively. n = 3 to 5 for each concentration.