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      Compartmentalized dendritic plasticity and input feature storage in neurons.

      Nature

      metabolism, genetics, deficiency, Shal Potassium Channels, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Rats, cytology, Pyramidal Cells, physiology, Neuronal Plasticity, Models, Neurological, Mice, Male, Ion Channel Gating, Dendrites, Cell Shape, Animals, Action Potentials

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          Abstract

          Although information storage in the central nervous system is thought to be primarily mediated by various forms of synaptic plasticity, other mechanisms, such as modifications in membrane excitability, are available. Local dendritic spikes are nonlinear voltage events that are initiated within dendritic branches by spatially clustered and temporally synchronous synaptic input. That local spikes selectively respond only to appropriately correlated input allows them to function as input feature detectors and potentially as powerful information storage mechanisms. However, it is currently unknown whether any effective form of local dendritic spike plasticity exists. Here we show that the coupling between local dendritic spikes and the soma of rat hippocampal CA1 pyramidal neurons can be modified in a branch-specific manner through an N-methyl-d-aspartate receptor (NMDAR)-dependent regulation of dendritic Kv4.2 potassium channels. These data suggest that compartmentalized changes in branch excitability could store multiple complex features of synaptic input, such as their spatio-temporal correlation. We propose that this 'branch strength potentiation' represents a previously unknown form of information storage that is distinct from that produced by changes in synaptic efficacy both at the mechanistic level and in the type of information stored.

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          Journal
          10.1038/nature06725
          18368112

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