| Summary: | 碩士 === 國立陽明大學 === 神經科學研究所 === 100 === Abstract of Part I
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 tri-synaptic circuit, is unclear. Recently, we found that GABAergic responses in adolescent and adult rat DGCs are still depolarizing from rest. To further elucidate how depolarizing GABA affects signal processing, we used a morphologically realistic DGC model to show that GABAergic action, depending on its precise timing and location, can have either an excitatory or inhibitory role in synaptic integration of dentate gyrus granule cells.
Abstract of Part II
Fast excitatory neurotransmission and synaptic plasticity occur at neuron-oligodendrocyte precursor cell (OPC) synapses. However, synaptic integration in these non-neuronal cells remains poorly understood. To determine how synaptic inputs integrate in OPCs, we combined dual whole-cell patch-clamp recordings with high-resolution two-photon microscopy to obtain anatomically detailed cable models of OPCs, in which K+ channel models developed from voltage-clamp data were implemented. Fits of passive voltage transients with multiple compartmental cable models based on morphology of the recorded cells revealed that OPCs have a relatively low specific axial resistivity (Ri ~63 Ωcm) and a very low specific membrane resistance (Rm~3.7 kΩcm2) compared with those of mammalian central neurons. Computational analysis of OPC cable models revealed that despite strong excitatory postsynaptic potential (EPSP) attenuation along dendrite-like processes, EPSP amplitude at the soma is much less dependent on synapse location. Intriguingly, somatic potential can efficiently spread to the entire cell upon synaptic activation. Notably, low Rm and Ri differentially restrict temporal summation of EPSPs, whereas large A-type K+ conductance substantially shortens spatially integrated EPSPs upon intense synaptic activation. Taken together, unique cable properties and A-type K+ conductance significantly limit spatiotemporal integration of synaptic inputs in OPCs.
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