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<i>Syngap1</i> regulates experience-dependent cortical ensemble plasticity by promoting in vivo excitatory synapse strengthening

Nerea Llamosas, Sheldon D. Michaelson, Thomas Vaissière, Camilo Rojas, Courtney A. Miller, Gavin Rumbaugh

2021Proceedings of the National Academy of Sciences20 citationsDOIOpen Access PDF

Abstract

Significance Many autism risk genes, such as Syngap1 , regulate synapse plasticity, and disruptions to this subcellular process are thought to underlie behavioral deficits. However, behavior emerges through experience-driven dynamics within neural ensembles or groups of coactivated neurons. It is currently unclear how genetic regulation of synapse plasticity contributes to experience-dependent changes to cortical ensemble activity. Our data demonstrate that disruptions to synapse-level strengthening mechanisms in Syngap1 mice underlies impairments to balanced plasticity within cortical ensembles driven by novel sensory experience. Because not all neurons in ensembles were sensitive to Syngap1 regulation, we propose that additional genetic mechanisms are also initiated in response to experience to effectively redistribute activity within cortical networks.

Topics & Concepts

NeuroscienceExcitatory postsynaptic potentialSynapseSynaptic plasticityMetaplasticityExcitatory synapseGlutamatergicNeuroplasticityLong-term potentiationNonsynaptic plasticityBiologyInhibitory postsynaptic potentialGlutamate receptorReceptorBiochemistryNeuroscience and Neural EngineeringNeural dynamics and brain functionAdvanced Fluorescence Microscopy Techniques