Presynaptic kainate receptors that enhance the release of GABA on CA1 hippocampal interneurons

We report that kainate receptors are present on presynaptic GABAergic termi nals contacting interneurons and that their activation increases GABA relea se. Application of kainate increased the frequency of miniature inhibitory postsynaptic currents recorded in CA1 interneurons. Local applications of g lutamate but not of AMPA or NMDA also increased GABA quantal release. Appli cation of kainate as well as synaptically released glutamate reduced the nu mber of failures of GABAergic neurotransmission between interneurons. Thus, activation of presynaptic kainate receptors increases the probability of G ABA release at interneuron-interneuron synapses. Glutamate may selectively control the communication between interneurons by increasing their mutual i nhibition.