4.3 Article

Activity-Dependent Changes in the Firing Properties of Neocortical Fast-Spiking Interneurons in the Absence of Large Changes in Gene Expression

Journal

DEVELOPMENTAL NEUROBIOLOGY
Volume 71, Issue 1, Pages 62-70

Publisher

WILEY
DOI: 10.1002/dneu.20811

Keywords

GABAergic interneuron; firing type; plasticity; intrinsic properties; cortex

Funding

  1. NINDS
  2. NIMH
  3. Simons Foundation
  4. NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH066338] Funding Source: NIH RePORTER

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The diverse cell types that comprise neocortical circuits each have characteristic integrative and firing properties that are specialized to perform specific functions within the network. Parvalbumin-positive fast-spiking (FS) interneurons are a particularly specialized cortical cell-type that controls the dynamics of ongoing activity and prevents runaway excitation by virtue of remarkably high firing rates, a feature that is permitted by narrow action potentials and the absence of spike-frequency adaptation. Although several neuronal intrinsic membrane properties undergo activity-dependent plasticity, the role of network activity in shaping and maintaining specialized, cell-type-specific firing properties is unknown. We tested whether the specialized firing properties of mature FS interneurons are sensitive to activity perturbations by inactivating a portion of motor cortex in vivo for 48 h and measuring resulting plasticity of FS intrinsic and firing properties with whole-cell recording in acute slices. Many of the characteristic properties of FS interneurons, including nonadapting high-frequency spiking and narrow action potentials, were profoundly affected by activity deprivation both at an age just after maturation of FS firing properties and also a week after their maturation. Using microarray screening, we determined that although normal maturation of FS electrophysiological specializations is accompanied by large-scale transcriptional changes, the effects of deprivation on the same specializations involve more modest transcriptional changes, and may instead be primarily mediated by post-transcriptional mechanisms. (C) 2010 Wiley Periodicals, Inc. Develop Neurobiol 71: 62-70, 2011

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