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

Author

Listed:
  • Naoki Takada

    (Cold Spring Harbor Laboratory)

  • Hyun Jae Pi

    (Cold Spring Harbor Laboratory)

  • Vitor H. Sousa

    (Smilow Neuroscience Program, New York University
    Present address: INMED, Inserm Unité 901, Marseille 13009, France)

  • Jack Waters

    (Feinberg School of Medicine, Northwestern University)

  • Gord Fishell

    (Smilow Neuroscience Program, New York University)

  • Adam Kepecs

    (Cold Spring Harbor Laboratory)

  • Pavel Osten

    (Cold Spring Harbor Laboratory)

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.

Suggested Citation

  • Naoki Takada & Hyun Jae Pi & Vitor H. Sousa & Jack Waters & Gord Fishell & Adam Kepecs & Pavel Osten, 2014. "A developmental cell-type switch in cortical interneurons leads to a selective defect in cortical oscillations," Nature Communications, Nature, vol. 5(1), pages 1-8, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6333
    DOI: 10.1038/ncomms6333
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