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Neuron DOI:10.1016/j.neuron.2014.06.033

Sensory integration in mouse insular cortex reflects GABA circuit maturation.

Publication TypeJournal Article
Year of Publication2014
AuthorsGogolla, N, Takesian, AE, Feng, G, Fagiolini, M, Hensch, TK
JournalNeuron
Volume83
Issue4
Pages894-905
Date Published2014 Aug 20
ISSN1097-4199
KeywordsAnimals, Autistic Disorder, Cerebral Cortex, Diazepam, Disease Models, Animal, GABAergic Neurons, Glutamate Decarboxylase, Male, Methyl-CpG-Binding Protein 2, Mice, Mice, Knockout, Nerve Tissue Proteins, Neural Pathways, Sensation, Species Specificity
Abstract

Insular cortex (IC) contributes to a variety of complex brain functions, such as communication, social behavior, and self-awareness through the integration of sensory, emotional, and cognitive content. How the IC acquires its integrative properties remains unexplored. We compared the emergence of multisensory integration (MSI) in the IC of behaviorally distinct mouse strains. While adult C57BL/6 mice exhibited robust MSI, this capacity was impaired in the inbred BTBR T+tf/J mouse model of idiopathic autism. The deficit reflected weakened γ-aminobutyric acid (GABA) circuits and compromised postnatal pruning of cross-modal input. Transient pharmacological enhancement by diazepam in BTBR mice during an early sensitive period rescued inhibition and integration in the adult IC. Moreover, impaired MSI was common across three other monogenic models (GAD65, Shank3, and Mecp2 knockout mice) displaying behavioral phenotypes and parvalbumin-circuit abnormalities. Our findings offer developmental insight into a key neural circuit relevant to neuropsychiatric conditions like schizophrenia and autism.

DOI10.1016/j.neuron.2014.06.033
Pubmed

http://www.ncbi.nlm.nih.gov/pubmed/25088363?dopt=Abstract

Alternate JournalNeuron
PubMed ID25088363
PubMed Central IDPMC4177076
Grant ListP50 MH094271 / MH / NIMH NIH HHS / United States
1P50MH094271 / MH / NIMH NIH HHS / United States
P30 HD018655 / HD / NICHD NIH HHS / United States
DP1 OD003699 / OD / NIH HHS / United States
DP1OD003699 / OD / NIH HHS / United States