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Transient developmental imbalance of cortical interneuron subtypes presages long-term changes in behavior.

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journal contribution
posted on 30.06.2021, 14:04 by Lorenza Magno, Zeinab Asgarian, Valentina Pendolino, Theodora Velona, Albert Mackintosh, Flora Lee, Agata Stryjewska, Celine Zimmer, François Guillemot, Mark Farrant, Beverley Clark, Nicoletta Kessaris
Cortical GABAergic interneurons are generated in large numbers in the ganglionic eminences and migrate into the cerebral cortex during embryogenesis. At early postnatal stages, during neuronal circuit maturation, autonomous and activity-dependent mechanisms operate within the cortex to adjust cell numbers by eliminating naturally occurring neuron excess. Here, we show that when cortical interneurons are generated in aberrantly high numbers-due to a defect in precursor cell proliferation during embryogenesis-extra parvalbumin interneurons persist in the postnatal mouse cortex during critical periods of cortical network maturation. Even though cell numbers are subsequently normalized, behavioral abnormalities remain in adulthood. This suggests that timely clearance of excess cortical interneurons is critical for correct functional maturation of circuits that drive adult behavior.

Funding

Crick (Grant ID: 10089, Grant title: Guillemot FC001089)

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