Caudally pronounced deficiencies in preplate splitting and migration underly a rostro-caudal progression of cortical lamination defects in the reeler brain

• Verfasst von: Moreno, Nieves Mingo [VerfasserIn]
• Verfasst von: Truschow, Pavel [VerfasserIn]
• Verfasst von: Staiger, Jochen F. [VerfasserIn]
• Verfasst von: Wagener, Jan Robin [VerfasserIn]
• Titel: Caudally pronounced deficiencies in preplate splitting and migration underly a rostro-caudal progression of cortical lamination defects in the reeler brain
• Verf.angabe: Nieves Mingo-Moreno, Pavel Truschow, Jochen F. Staiger, Robin J. Wagener
• E-Jahr: 2024
• Jahr: February 2024
• Umfang: 20 S.
• Illustrationen: Illustrationen
• Fussnoten: Gesehen am 14.01.2025
• Titel Quelle: Enthalten in: Cerebral cortex
• Ort Quelle: Oxford : Oxford Univ. Press, 1991
• Jahr Quelle: 2024
• Band/Heft Quelle: 34(2024), 2 vom: Feb., Artikel-ID bhae023, Seite 1-20
• ISSN Quelle: 1460-2199
• DOI: doi:10.1093/cercor/bhae023
• Datenträger: Online-Ressource
• Sprache: eng
• K10plus-PPN: 1914590392

Abstract

In mammalian neocortex development, every cohort of newborn neurons is guided toward the marginal zone, leading to an “inside-out” organization of the 6 neocortical layers. This migratory pattern is regulated by the extracellular glycoprotein Reelin. The reeler mouse shows a homozygous mutation of the reelin gene. Using RNA in situ hybridization we could demonstrate that the Reelin-deficient mouse cortex (male and female) displays an increasing lamination defect along the rostro-caudal axis that is characterized by strong cellular intermingling, but roughly reproduces the “inside-out” pattern in rostral cortex, while caudal cortex shows a relative inversion of neuronal positioning (“outside-in”). We found that in development of the reeler cortex, preplate-splitting is also defective with an increasing severity along the rostro-caudal axis. This leads to a misplacement of subplate neurons that are crucial for a switch in migration mode within the cortical plate. Using Flash Tag labeling and nucleoside analog pulse-chasing, we found an according migration defect within the cortical plate, again with a progressive severity along the rostro-caudal axis. Thus, loss of one key player in neocortical development leads to highly area-specific (caudally pronounced) developmental deficiencies that result in multiple roughly opposite rostral versus caudal adult neocortical phenotypes.