Decrease of SYNGAP1 in GABAergic cells impairs inhibitory synapse connectivity, synaptic inhibition and cognitive function

Martin H. Berryer, Bidisha Chattopadhyaya, Paul Xing, Ilse Riebe, Ciprian Bosoi, Nathalie Sanon, Judith Antoine-Bertrand, Maxime Lévesque, Massimo Avoli, Fadi F. Hamdan, Lionel Carmant, Nathalie Lamarche-Vane, Jean-Claude Lacaille, Jacques L. Michaud () and Graziella Di Cristo ()
Additional contact information
Martin H. Berryer: Université de Montréal
Bidisha Chattopadhyaya: Université de Montréal
Paul Xing: Université de Montréal
Ilse Riebe: Université de Montréal
Ciprian Bosoi: CHU Sainte-Justine Research Center
Nathalie Sanon: CHU Sainte-Justine Research Center
Judith Antoine-Bertrand: Cancer Research Program of the Research Institute of MUHC, McGill University
Maxime Lévesque: Montreal Neurological Institute, McGill University
Massimo Avoli: Montreal Neurological Institute, McGill University
Fadi F. Hamdan: CHU Sainte-Justine Research Center
Lionel Carmant: Université de Montréal
Nathalie Lamarche-Vane: Cancer Research Program of the Research Institute of MUHC, McGill University
Jean-Claude Lacaille: Université de Montréal
Jacques L. Michaud: Université de Montréal
Graziella Di Cristo: Université de Montréal

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Haploinsufficiency of the SYNGAP1 gene, which codes for a Ras GTPase-activating protein, impairs cognition both in humans and in mice. Decrease of Syngap1 in mice has been previously shown to cause cognitive deficits at least in part by inducing alterations in glutamatergic neurotransmission and premature maturation of excitatory connections. Whether Syngap1 plays a role in the development of cortical GABAergic connectivity and function remains unclear. Here, we show that Syngap1 haploinsufficiency significantly reduces the formation of perisomatic innervations by parvalbumin-positive basket cells, a major population of GABAergic neurons, in a cell-autonomous manner. We further show that Syngap1 haploinsufficiency in GABAergic cells derived from the medial ganglionic eminence impairs their connectivity, reduces inhibitory synaptic activity and cortical gamma oscillation power, and causes cognitive deficits. Our results indicate that Syngap1 plays a critical role in GABAergic circuit function and further suggest that Syngap1 haploinsufficiency in GABAergic circuits may contribute to cognitive deficits.

Date: 2016
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DOI: 10.1038/ncomms13340

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