The hilus is a part of the hippocampal formation, which is a structure important for formation of memories. There, granule cells (GCs) form a gateway to the hippocampus, filtering incoming sensory information. GCs project into the hilus (GC axons are called mossy fibers; MFs) and synapse onto hilar mossy cells (HMCs), that project back onto GCs forming a recurrent circuit. Feed-forward inhibition from HMCs to GCs via subpopulations of hilar interneurons serves as a brake on this recurrent excitatory circuit. Kainate receptors are expressed by hilar neurons; elsewhere in the hippocampus, these receptors alter synaptic strength as well as intrinsic cellular excitability via both ionotropic and metabotropic functions. We hypothesize that kainate receptors at excitatory synapses in the hilus also modulate network excitability and that aberrant function might therefore lead to network hyperexcitability relevant to seizures and epilepsy. These questions will be considered using primarily a electrophysiological approach that utilizes selective pharmacological compounds, optogenetics, and gene-targeted mice lacking one or more kainate receptor subunits.