Kainate receptor activation affects GABAergic inhibition in the hippocampus
by mechanisms that are thought to involve the GluR5 subunit. We report tha
t disruption of the GluR5 subunit gene does not cause the loss of functiona
l KARs in CA1 interneurons, nor does it prevent kainate-induced inhibition
of evoked GABAergic synaptic transmission onto CA1 pyramidal cells. However
, KAR function is abolished in mice lacking both GluR5 and GluR6 subunits,
indicating that KARs in CA1 stratum radiatum interneurons are heteromeric r
eceptors composed of both subunits. In addition, we show the presence of pr
esynaptic KARs comprising the GluR6 but not the GluR5 subunit that modulate
synaptic transmission between inhibitory interneurons. The existence of tw
o separate populations of KARs in hippocampal interneurons adds to the comp
lexity of KAR localization and function.