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

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

Nature communications (2014-10-31)
Naoki Takada, Hyun Jae Pi, Vitor H Sousa, Jack Waters, Gord Fishell, Adam Kepecs, Pavel Osten
ANOTACE

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.

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Sigma-Aldrich
Somatostatin, powder, BioReagent, suitable for cell culture
Sigma-Aldrich
Somatostatin, ≥97% (HPLC), powder
Somatostatin, European Pharmacopoeia (EP) Reference Standard