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. 2013 Jan;83(1):106–121. doi: 10.1124/mol.112.081802

Fig. 4.

Fig. 4.

Potentiation of heteromeric KARs by group I mGlu activation. (A) whole-cell currents were recorded from oocytes 3 days after injection with mRNAs encoding GluK2/mGlu1, GluK2/GluK4/mGlu1, or GluK2/GluK5/mGlu1. After application of 100 µM ACPD (a nonspecific mGlu activator), steady-state activation of the heteromeric receptors by AMPA (30 µM) was potentiated, but not steady-state activation of the homomeric KAR by domoic acid (10 µM). (B) time-dependent potentiation of GluK2/GluK4/mGlu1 and GluK2/GluK5/mGlu1 AMPA currents by mGlu1 activation with ACPD (n = 5 and n = 16, respectively). (C) varying the subunit combination of the KAR and mGlu receptors revealed significant ACPD potentiation of only the heteromeric KARs expressed together with group I mGlu receptors (n ≥ 4). The largest ACPD-mediated potentiation was seen in oocytes expressing GluK2/GluK5/mGlu1 (n = 16) (*P < 0.05, **P < 0.01, ***P < 0.005, ****P < 0.0001, ns=not significant; one-way ANOVA with selected Bonferroni’s post-tests). (D) AMPA concentration-response curves from oocytes expressing GluK2/GluK5/mGlu1 before and after mGlu activation revealed potentiation at multiple AMPA concentrations with no apparent difference in the concentration ranges over which kainate receptors are activated and desensitized (n = 4).