A developmental cell-type switch in cortical interneurons leads to a selective defect in cortical oscillations

Nat Commun. 2014 Oct 30:5:5333. doi: 10.1038/ncomms6333.

Abstract

The cellular diversity of interneurons in the neocortex is thought to reflect subtype-specific roles of cortical inhibition. Here we ask whether perturbations to two subtypes--parvalbumin-positive (PV+) and somatostatin-positive (SST+) interneurons--can be compensated for with respect to their contributions to cortical development. We use a genetic cell fate switch to delete both PV+ and SST+ interneurons selectively in cortical layers 2-4 without numerically changing the total interneuron population. This manipulation is compensated for at the level of synaptic currents and receptive fields (RFs) in the somatosensory cortex. By contrast, we identify a deficit in inhibitory synchronization in vitro and a large reduction in cortical gamma oscillations in vivo. This reveals that, while the roles of inhibition in establishing cortical inhibitory/excitatory balance and RFs can be subserved by multiple interneuron subtypes, gamma oscillations depend on cellular properties that cannot be compensated for--likely, the fast signalling properties of PV+ interneurons.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cortical Synchronization*
  • In Vitro Techniques
  • Interneurons / physiology*
  • Male
  • Mice
  • Neocortex / physiology*
  • Nuclear Proteins / deficiency
  • Parvalbumins / deficiency
  • Patch-Clamp Techniques
  • Pyramidal Cells / physiology*
  • Somatostatin / deficiency
  • Thyroid Nuclear Factor 1
  • Transcription Factors / deficiency

Substances

  • Nuclear Proteins
  • Parvalbumins
  • Thyroid Nuclear Factor 1
  • Transcription Factors
  • Somatostatin