In the neonatal hippocampus, the activity of interneurons shapes early network bursts that are important for the establishment of neuronal connectivity. However, mechanisms controlling the firing of immature interneurons remain elusive. We now show that the spontaneous firing rate of CA3 stratum lucidum interneurons markedly decreases during early postnatal development, due to changes in the properties of GluR5-subunit containing kainate receptors (KARs). In the neonate, activation of KARs by ambient glutamate exerts a tonic inhibition of the medium-duration afterhyperpolarization (mAHP) by a G-protein dependent mechanism, permitting high interneuronal firing rate. During development, the amplitude of the apamine sensitive K+ currents responsible for the mAHP increases dramatically due to decoupling between KAR activation and mAHP modulation, leading to decreased interneuronal firing. The developmental shift in the KAR function and its consequences on interneuronal activity might have a fundamental role in the maturation of the synchronous neuronal oscillations typical for adult hippocampal circuitry.

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