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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. 10.

Fig. 10

Binding affinity at GluR5-2a subunits correlates with seizure activity. Linear correlation graph is plotted as Ki (nanomolar) versus ED50 (picomoles per mouse) after i.c.v. injection of the following compounds: DH (13 pmol/mouse), neoDH (16 pmol/mouse), MSVIII-19 (6.3 nmol/mouse), 8-deoxy-neoDH (238 pmol/mouse), 9-deoxy-neoDH (7.1 nmol/mouse), 8-epi-neoDH (283 pmol/mouse), 9-epi-neoDH (8.6 nmol/mouse), 9-F-8-epi-neoDH (374 pmol/mouse), 2,4-epi-neoDH (11.4 nmol/mouse), and 4-epi-neoDH (1.7 nmol/mouse) (Shoji et al., 2006). These data show a correlation (r = 0.86; p < 0.01) for binding affinity of analogs for GluR5-2a KAR subunits. A much weaker correlation between seizure activity and binding affinity for GluR6a subunits of a subset of analogs was noted (r = 0.74; p = 0.095); several compounds could not be included in this analysis because they do not exhibit measurable affinity for this receptor subunit (i.e., MSVIII-19, 9-deoxy-neoDH, 9-epi-neoDH, and 9-F-8-epi-neoDH). Likewise, no correlation analysis was possible with GluR7a, KA2, or AMPA receptor subunits because of the absence of binding affinity.