Abstract

Sensory cortical plasticity is usually quantified by changes in evoked firing rate. In this study we quantified plasticity by changes in sensory detection performance using Chernoff information and receiver operating characteristic analysis. We found that whisker deprivation causes a change in information flow within the cortical layers and that layer 5 regular-spiking cells, despite showing only a small potentiation of short-latency input, show the greatest increase in information content for the spared input partly by decreasing their spontaneous activity.

Highlights

  • NEW & NOTEWORTHY Sensory cortical plasticity is usually quantified by changes in evoked firing rate

  • What mechanisms might be responsible for the different reactions of different cell types to the same deprivation pattern? At the cellular level, these include different capacities between cells for particular synaptic plasticity processes such as long-term potentiation (LTP), long-term depression (LTD), and homeostatic plasticity; at the circuit level, these include the dynamic interaction between cells in different layers of the cortical columns, the relative strength of cortical vs. thalamic input differences, and changes in the balance between excitatory and inhibitory inputs

  • layer 5 (L5) cells were further classified as intrinsically bursting (L5IB) or regular spiking (L5RS) according to their firing pattern in response to current injection, and the classes correlated with their morphology (Fig. 1, D and E; Jacob et al 2012)

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Summary

Introduction

NEW & NOTEWORTHY Sensory cortical plasticity is usually quantified by changes in evoked firing rate. Field plasticity is known to vary with the type of sensory modification set by the experimenters, but for any given pattern of deprivation, the plasticity is relatively uniform in effect across neurons (Feldman and Brecht 2005; Wallace and Fox 1999). We recently found that a row-deprivation pattern can cause nonuniform receptive field plasticity in subtypes of layer 5 (L5) pyramidal cells (Jacob et al 2012). These include different capacities between cells for particular synaptic plasticity processes such as long-term potentiation (LTP), long-term depression (LTD), and homeostatic plasticity; at the circuit level, these include the dynamic interaction between cells in different layers of the cortical columns, the relative strength of cortical vs thalamic input differences, and changes in the balance between excitatory and inhibitory inputs. In this study we have concentrated on the differences that might arise at the circuit level

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