GABAergic signaling in hippocampal pyramidal neurons undergoes a switch from depolarizing to hyperpolarizing during early neuronal development. Whether such a transformation of GABAergic action occurs in dentate granule cells (DGCs), located at the first stage of the hippocampal trisynaptic circuit, is unclear. Here, we use noninvasive extracellular recording to monitor the effect of synaptically released GABA on the DGC population. We find that GABAergic responses in adolescent and adult rat DGCs are still depolarizing from rest. Using a morphologically realistic DGC model, we show that GABAergic action, depending on its precise timing and location, can have either an excitatory or inhibitory role in signal processing in the dentate gyrus.

Key points• We developed detailed passive cable models of rat oligodendrocyte precursor cells (OPCs) based on dual somatic recordings and complete morphological reconstructions.• Both specific membrane capacitance and specific axial resistivity are comparable to those of central neurons, but the average specific membrane resistance (R m ∼4.1 k cm 2 ) is substantially lower in OPCs.• Large Ba 2+ -and bupivacaine-sensitive background K + conductances contribute to the low R m .• Simultaneous dual soma and process whole-cell recordings reveal powerful voltage attenuation along OPC processes, indicating that OPC processes are a strong voltage attenuator.• The low R m also sharpens EPSPs and thus narrows the temporal window for EPSP integration.Abstract Glutamatergic transmission onto oligodendrocyte precursor cells (OPCs) may regulate OPC proliferation, migration and differentiation. Dendritic integration of excitatory postsynaptic potentials (EPSPs) is critical for neuronal functions, and mechanisms regulating dendritic propagation and summation of EPSPs are well understood. However, little is known about EPSP attenuation and integration in OPCs. We developed realistic OPC models for synaptic integration, based on passive membrane responses of OPCs obtained by simultaneous dual whole-cell patch-pipette recordings. Compared with neurons, OPCs have a very low value of membrane resistivity, which is largely mediated by Ba 2+ -and bupivacaine-sensitive background K + conductances. The very low membrane resistivity not only leads to rapid EPSP attenuation along OPC processes but also sharpens EPSPs and narrows the temporal window for EPSP summation. Thus, background K + conductances regulate synaptic responses and integration in OPCs, thereby affecting activity-dependent neuronal control of OPC development and function.