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<PubmedArticle><MedlineCitation Status="MEDLINE" Owner="NLM" IndexingMethod="Manual"><PMID Version="1">24723342</PMID><DateCompleted><Year>2015</Year><Month>03</Month><Day>30</Day></DateCompleted><DateRevised><Year>2014</Year><Month>07</Month><Day>24</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1097-0177</ISSN><JournalIssue CitedMedium="Internet"><Volume>243</Volume><Issue>8</Issue><PubDate><Year>2014</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Developmental dynamics : an official publication of the American Association of Anatomists</Title><ISOAbbreviation>Dev Dyn</ISOAbbreviation></Journal><ArticleTitle>The zinc finger gene Fezf2 is required for the development of excitatory neurons in the basolateral complex of the amygdala.</ArticleTitle><Pagination><StartPage>1030</StartPage><EndPage>1036</EndPage><MedlinePgn>1030-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/dvdy.24137</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">The basolateral complex, comprised of the lateral, basolateral, and basomedial nuclei, is the main structure of the amygdala and contains two neuronal cell types: excitatory neurons and inhibitory interneurons. Studies show that most of the excitatory neurons originate in the ventral pallium of the telencephalon. However, their subsequent development remains poorly understood.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">In this study, we examined the roles of the zinc finger gene Fezf2 in the development of the amygdala. Fezf2 is expressed in the lateral and basolateral nuclei during development. In Fezf2-deficient embryos, specific excitatory neuron markers in the lateral and basolateral nuclei were reduced, with concurrent induction of other markers in the endopiriform cortex. Furthermore, the morphology of the lateral and basolateral nuclei was abnormal. In the adult stages, excitatory neurons in the lateral and basolateral nuclei were greatly reduced because of apoptosis that occurred soon after birth.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">These results suggest that Fezf2 is required for the development of excitatory neurons and nuclear morphology in the lateral and basolateral nuclei, and that abnormal formation of these regions leads to cell death soon after birth in Fezf2-deficient mice.</AbstractText><CopyrightInformation>&#xa9; 2014 Wiley Periodicals, Inc.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hirata-Fukae</LastName><ForeName>Chiho</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Senior Research Fellow Center, Ehime University, Ehime, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hirata</LastName><ForeName>Tsutomu</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>05</Month><Day>02</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Dev Dyn</MedlineTA><NlmUniqueID>9201927</NlmUniqueID><ISSNLinking>1058-8388</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000679" MajorTopicYN="N">Amygdala</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013687" MajorTopicYN="N">Telencephalon</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Fezf2</Keyword><Keyword MajorTopicYN="N">amygdale</Keyword><Keyword MajorTopicYN="N">basolateral complex</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2013</Year><Month>12</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2014</Year><Month>4</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>4</Month><Day>6</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>4</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>4</Month><Day>12</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>3</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24723342</ArticleId><ArticleId IdType="doi">10.1002/dvdy.24137</ArticleId></ArticleIdList></PubmedData></PubmedArticle></PubmedArticleSet>