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Goff-et-al-2023

This is the accompanying source dataset and associated original code to the manuscript published in Cell Reports 2023: VIP interneuron impairment promotes in vivo circuit dysfunction and autism-related behaviors in Dravet syndrome. Kevin M. Goff, Sophie R. Liebergall, Evan Jiang, Ala Somarowthu, and Ethan M. Goldberg

Preprocessed 2P imaging data provided in .mat file format for analysis in Matlab (2021a or newer). The function MI_values.m produces the modulation index values that we report in the paper and form the basis of our conclusions.

Additional files for analysis are provided with the preprocessed data to generate the main panels from each figure. Each figure has one associated zip file that includes both a script and the data required to generate each figure.

Any additional analysis from supplemental figures available upon request from the coresponding author.

Many figures are generated with gramm for Matlab (doi: 10.21105/joss.00568) which will need to be added to the matlab path prior to running the scripts

datacite.yml
Title	Goff-et-al-2023 VIP interneuron impairment promotes in vivo circuit dysfunction and autism-related behaviors in Dravet syndrome
Authors	Goff,Kevin;The University of Pennsylvania School of Medicine;ORCID:0000-0001-5862-0219 Somarowthu,Ala;The Children's Hospital of Philadelphia Goldberg,Ethan;The Children's Hospital of Philadelphia;ORCID:0000-0002-7404-735X
Description	Dravet Syndrome (DS) is a severe neurodevelopmental disorder caused by loss of function variants in SCN1A which encodes the voltage-gated sodium channel subunit Nav1.1. We recently showed that neocortical vasoactive intestinal peptide interneurons (VIP-INs) express Nav1.1 and are hypoexcitable in DS (Scn1a+/-) mice. Here, we investigated VIP-IN function at the circuit and behavioral level by performing in vivo 2-photon calcium imaging in awake WT and Scn1a+/- mice. VIP-IN and pyramidal neuron activation during behavioral transition from quiet wakefulness to active running was diminished in Scn1a+/- mice, and optogenetic activation of VIP-INs restored pyramidal neuron activity to WT levels during locomotion. VIP-IN selective Scn1a deletion reproduced core autism spectrum disorder-related behaviors in addition to cellular- and circuit-level deficits in VIP-IN function, but without epilepsy, sudden death, or avoidance behaviors seen in the global model. Hence, VIP-INs are impaired in vivo and may underlie non-seizure cognitive and behavioral comorbidities in DS.
License	Creative Commons CC0 1.0 Public Domain Dedication (https://creativecommons.org/publicdomain/zero/1.0/)
References	Goff, K. M. & Goldberg, E. M. VIP interneuron impairment promotes in vivo circuit dysfunction and autism-related behaviors in Dravet syndrome. Cell Reports (Accepted, 2023). [] (IsSupplementTo)
Funding	NIH NINDS, F31 NS111803 NIH NINDS, R01 NS110869 The Dana Foundation, David Mahoney Neuroimaging Program Burroughs Wellcome Fund, Career Award for Medical Scientists
Keywords	Dravet syndrome SCN1A VIP Interneuron Autism Optogenetics Two-photon imaging
Resource Type	Dataset

README.md

Goff-et-al-2023