{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T09:50:20Z","timestamp":1782294620258,"version":"3.54.5"},"reference-count":36,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2018,7,10]],"date-time":"2018-07-10T00:00:00Z","timestamp":1531180800000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2018,7,1]],"date-time":"2018-07-01T00:00:00Z","timestamp":1530403200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["MH066332"],"award-info":[{"award-number":["MH066332"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J of Neuroscience"],"published-print":{"date-parts":[[2018,7]]},"abstract":"Abstract<\/jats:title>\n \n To explore roles for ephrin\u2010B\/EphB signaling in cortical interneurons, we previously generated\n ephrin\u2010B<\/jats:italic>\n (\n Efnb1\/b2\/b3<\/jats:italic>\n ) conditional triple mutant (\n \n TM<\/jats:styled-content>\n <\/jats:italic>\n lz<\/jats:sup>\n ) mice using a Dlx1\/2.Cre inhibitory neuron driver and green fluorescent protein (\n GFP<\/jats:styled-content>\n ) reporters for the two main inhibitory interneuron groups distinguished by expression of either glutamic acid decarboxylase 1 (\n GAD<\/jats:styled-content>\n 1;\n GAD<\/jats:styled-content>\n 67\u2010\n GFP<\/jats:styled-content>\n ) or 2 (\n GAD<\/jats:styled-content>\n 2;\n GAD<\/jats:styled-content>\n 65\u2010\n GFP<\/jats:styled-content>\n ). This work showed a general involvement of ephrin\u2010B in migration and population of interneurons into the embryonic neocortex. We now determined whether specific interneurons are selectively affected in the adult brains of\n \n TM<\/jats:styled-content>\n <\/jats:italic>\n lz<\/jats:sup>\n .Cre mice by immunostaining with antibodies that identify the different subtypes. The results indicate that\n GAD<\/jats:styled-content>\n 67\u2010\n GFP<\/jats:styled-content>\n \u2010expressing interneurons that also express parvalbumin (\n PV<\/jats:styled-content>\n ), calretinin (\n CR<\/jats:styled-content>\n ) and, to a lesser extent, somatostatin (\n SST<\/jats:styled-content>\n ) and Reelin (Rln) were significantly reduced in the cortex and hippocampal\n CA<\/jats:styled-content>\n 1 region in\n \n TM<\/jats:styled-content>\n <\/jats:italic>\n lz<\/jats:sup>\n .Cre mutant mice. Neuropeptide Y (\n NPY<\/jats:styled-content>\n ) interneurons that also express\n GAD<\/jats:styled-content>\n 67\u2010\n GFP<\/jats:styled-content>\n were reduced in the hippocampal\n CA<\/jats:styled-content>\n 1 region, but much less so in the cortex, although these cells exhibited abnormal cortical layering. In\n GAD<\/jats:styled-content>\n 65\u2010\n GFP<\/jats:styled-content>\n \u2010expressing interneurons,\n CR<\/jats:styled-content>\n subtypes were reduced in both cortex and hippocampal\n CA<\/jats:styled-content>\n 1 region, whereas Rln interneurons were reduced exclusively in hippocampus, and the numbers of\n NPY<\/jats:styled-content>\n and vasoactive intestinal polypeptide (\n VIP<\/jats:styled-content>\n ) subtypes appeared normal.\n PV<\/jats:styled-content>\n and\n CR<\/jats:styled-content>\n subtype interneurons in\n \n TM<\/jats:styled-content>\n <\/jats:italic>\n lz<\/jats:sup>\n .Cre mice also exhibited reductions in their perisomatic area, suggesting abnormalities in dendritic\/axonal complexity. Altogether, our data indicate that ephrin\u2010B expression within forebrain interneurons is required in specific subtypes for their normal population, cortical layering and elaboration of cell processes.\n <\/jats:p>","DOI":"10.1111\/ejn.14022","type":"journal-article","created":{"date-parts":[[2018,6,15]],"date-time":"2018-06-15T00:26:01Z","timestamp":1529022361000},"page":"1803-1817","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Abnormalities in cortical interneuron subtypes in ephrin\u2010B mutant mice"],"prefix":"10.1111","volume":"48","author":[{"given":"Asghar","family":"Talebian","sequence":"first","affiliation":[{"name":"Department of Neuroscience and Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration University of Texas Southwestern Medical Center Dallas Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6741-4927","authenticated-orcid":false,"given":"Rachel","family":"Britton","sequence":"additional","affiliation":[{"name":"Department of Neuroscience and Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration University of Texas Southwestern Medical Center Dallas Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7525-1061","authenticated-orcid":false,"given":"Mark","family":"Henkemeyer","sequence":"additional","affiliation":[{"name":"Department of Neuroscience and Kent Waldrep Center for Basic Research on Nerve Growth and Regeneration University of Texas Southwestern Medical Center Dallas Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,7,10]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.mcn.2008.01.006"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.3389\/fncel.2015.00393"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1535-7597.2003.03208.x"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1101\/gad.1171704"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1159\/000334489"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neuropharm.2012.08.015"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-8993(97)00683-5"},{"key":"e_1_2_10_9_1","doi-asserted-by":"publisher","DOI":"10.1111\/(ISSN)1460-9568"},{"key":"e_1_2_10_10_1","doi-asserted-by":"publisher","DOI":"10.1242\/dev.129.6.1397"},{"key":"e_1_2_10_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn1787"},{"key":"e_1_2_10_12_1","doi-asserted-by":"crossref","first-page":"269","DOI":"10.31887\/DCNS.2009.11.3\/dalewis","article-title":"Neuroplasticity of excitatory and inhibitory cortical circuits in schizophrenia","volume":"11","author":"Lewis D. 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