Ba2+‐ and bupivacaine‐sensitive background K+ conductances mediate rapid EPSP attenuation in oligodendrocyte precursor cells
Published online on September 10, 2013
Abstract
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We developed detailed passive cable models of rat oligodendrocyte precursor cells (OPCs) based on dual somatic recordings and complete morphological reconstructions.
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Both specific membrane capacitance and specific axial resistivity are comparable to those of central neurons, but the average specific membrane resistance (Rm∼4.1 kΩ cm2) is substantially lower in OPCs.
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Large Ba2+‐ and bupivacaine‐sensitive background K+ conductances contribute to the low Rm.
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Simultaneous dual soma and process whole‐cell recordings reveal powerful voltage attenuation along OPC processes, indicating that OPC processes are a strong voltage attenuator.
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The low Rm 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 Ba2+‐ 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.