作者: Y.-D. Zhou , C. D. Acker , T. I. Netoff , K. Sen , J. A. White
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摘要: Repeated induction of pre- and postsynaptic action potentials (APs) at a fixed time difference leads to long-term potentiation (LTP) or depression (LTD) the synapse, depending on temporal order activity. This phenomenon spike-timing-dependent plasticity (STDP) is believed arise by nonlinear processes that lead larger calcium transients (and thus LTP) when presynaptic APs precede smaller LTD) APs. In contrast predictions from such calcium-peak-detector models, we show constitutively artificially broadened in layer II/III pyramidal cells entorhinal cortex (EC) an increase dendritic transient shift balance STDP toward LTD. NMDA-receptor-dependent modulated CaV1Ca2+ channel-blocker nifedipine. Results are consistent with elaboration model which downstream signals voltage-dependent Ca2+ channels suppress LTP relative Our results suggest modulation AP width potent way adjust rules synaptic EC.