{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,9]],"date-time":"2025-10-09T01:08:08Z","timestamp":1759972088487,"version":"build-2065373602"},"reference-count":42,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2006,1,24]],"date-time":"2006-01-24T00:00:00Z","timestamp":1138060800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Anat. Rec."],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>GAP\u201043 heterozygous (HZ) mice exhibit abnormal thalamocortical pathfinding, fasciculation, and terminal arborization at postnatal day 7 (P7). Here we tested whether these defects are correlated with delayed development of HZ cortical patterns. We assessed the rate of barrel segregation and radial glia differentiation in wild\u2010type (WT) and HZ cortices. Since GAP\u201043 is involved in some forms of neural plasticity, we also compared the duration of the critical period for lesion\u2010induced plasticity in both genotypes. Cytochrome oxidase histochemistry revealed a delay of approximately 1 day in barrel pattern formation in GAP\u201043 HZ mice. GAP\u201043 WT barrels showed complete segregation between P2\u2013P3, while HZ barrels did not reach the same level of segregation until P3\u2013P4. We found a similar delay in the transformation of radial glia from monopolar to multipolar phenotypes, from P5 in WT to P7 in HZ cortex. Radial glial cells represent many of the neuronal progenitors in developing cortex and aid in cell migration. Thus, the delay in radial glial differentiation may contribute to the delay in HZ barrel segregation. Interestingly, we found no change in the extent of the critical period for HZ cortical responsiveness to early peripheral damage or in the time course of the cortical response. As expected, GAP\u201043 expression in HZ cortex is significantly reduced early in development. However, HZ GAP\u201043 expression remains at maximum levels after P9, when it is normally downregulated. As a result, HZ GAP\u201043 expression is near\u2010normal by P26, by which time near\u2010normal barrel dimensions have been restored. Our findings indicate that GAP\u201043 deficiency leads to early delays in barrel development and suggest that these failures are followed by homeostatic responses, including prolonged GAP\u201043 expression. These compensatory mechanisms may rescue normal cortical reorganization in neonates and near\u2010normal barrel morphology and GAP\u201043 expression in adulthood. \u00a9 2006 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/ar.a.20291","type":"journal-article","created":{"date-parts":[[2006,1,24]],"date-time":"2006-01-24T16:45:09Z","timestamp":1138121109000},"page":"143-157","source":"Crossref","is-referenced-by-count":7,"title":["GAP\u201043 heterozygous mice show delayed barrel patterning, differentiation of radial glia, and downregulation of GAP\u201043"],"prefix":"10.1002","volume":"288A","author":[{"given":"Vera","family":"McIlvain","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James 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