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Acute knockdown of the \u03b1\u2010subunit (G\u03b1i2) with <jats:italic>in utero<\/jats:italic> electroporation caused delayed radial migration of excitatory neurons during corticogenesis, perhaps because of impaired morphology. The migration phenotype was rescued by an <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>i\u2010resistant version of G\u03b1i2. On the other hand, silencing of G\u03b1i2 did not affect axon elongation, dendritic arbor formation or neurogenesis at ventricular zone <jats:italic>in\u00a0vivo<\/jats:italic>. When behavior analyses were conducted with acute G\u03b1i2\u2010knockdown mice, they showed defects in social interaction, novelty recognition and active avoidance learning as well as increased anxiety. Subsequently, using whole\u2010exome sequencing analysis, we identified a <jats:italic>de novo<\/jats:italic> heterozygous missense mutation (c.680C&gt;T; p.Ala227Val) in the <jats:italic><jats:styled-content style=\"fixed-case\">GNAI<\/jats:styled-content>2<\/jats:italic> gene encoding G\u03b1i2 in an individual with periventricular nodular heterotopia and intellectual disability. Collectively, the phenotypes in the knockdown experiments suggest a role of G\u03b1i2 in the brain development, and impairment of its function might cause defects in neuronal functions which lead to neurodevelopmental disorders.<\/jats:p><\/jats:sec><jats:sec><jats:label\/><jats:p>\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc13878-fig-0010-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>\n<\/jats:p><\/jats:sec>","DOI":"10.1111\/jnc.13878","type":"journal-article","created":{"date-parts":[[2016,11,29]],"date-time":"2016-11-29T09:09:10Z","timestamp":1480410550000},"page":"82-95","source":"Crossref","is-referenced-by-count":24,"title":["Role of a heterotrimeric G\u2010protein, Gi2, in the corticogenesis: possible involvement in periventricular nodular heterotopia and intellectual disability"],"prefix":"10.1111","volume":"140","author":[{"given":"Nanako","family":"Hamada","sequence":"first","affiliation":[{"name":"Department of Molecular Neurobiology Institute for Developmental Research Aichi Human Service Center Kasugai Japan"},{"name":"Research Fellow of Japan Society for the Promotion of Science Tokyo Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yutaka","family":"Negishi","sequence":"additional","affiliation":[{"name":"Department of Pediatrics and Neonatology Nagoya City University Graduate School of Medical Sciences Nagoya Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Makoto","family":"Mizuno","sequence":"additional","affiliation":[{"name":"Department of Molecular Neurobiology Institute for Developmental Research Aichi Human Service Center Kasugai 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