RT info:eu-repo/semantics/article
T1 Cajal-Retzius neurons are required for the development of the human hippocampal fissure.
A1 González Gómez, Miriam
A1 Meyer, Gundela
A1 Gonzalez-Arnay, Emilio
A1 Moll, Ute
A1 Nemajerova, Alice
A1 Tissir, Fadel
K1 Choroid plexus
K1 Cortical hem
K1 Meninges
AB Cajal-Retzius neurons (CRN) are the main source of Reelin in the marginal zone of the developing neocortexand hippocampus (HC). They also express the transcription factor p73 and are complemented by laterappearing GABAergic Reelin+ interneurons. The human dorsal HC forms at gestational week 10 (GW10), whenit develops a rudimentary Ammonic plate and incipient dentate migration, although the dorsal hippocampalfissure (HF) remains shallow and contains few CRN. The dorsal HC transforms into the indusium griseum (IG),concurrently with the rostro-caudal appearance of the corpus callosum, by GW14–17. Dorsal and ventral HCmerge at the site of the former caudal hem, which is located at the level of the future atrium of the lateralventricle and closely connected with the choroid plexus. The ventral HC forms at GW11 in the temporal lobe.The ventral HF is wide open at GW14–16 and densely populated by large numbers of CRNs. These are inintimate contact with the meninges and meningeal blood vessels, suggesting signalling through diversepathways. At GW17, the fissure deepens and begins to fuse, although it is still marked by p73/Reelin+ CRNs.The p73KO mouse illustrates the importance of p73 in CRN for HF formation. In the mutant, Tbr1/Reelin+ CRNsare born in the hem but do not leave it and subsequently disappear, so that the mutant cortex and HC lackCRN from the onset of corticogenesis. The HF is absent, which leads to profound architectonic alterations ofthe HC. To determine which p73 isoform is important for HF formation, isoform-specific TAp73- and DeltaNp73-deficient embryonic and early postnatal mice were examined. In both mutants, the number of CRNs wasreduced, but each of their phenotypes was much milder than in the global p73KO mutant missing bothisoforms. In the TAp73KO mice, the HF of the dorsal HC failed to form, but was present in the ventral HC. Inthe DeltaNp73KO mice, the HC had a mild patterning defect along with a shorter HF. Complex interactionsbetween both isoforms in CRNs may contribute to their crucial activity in the developing brain.
SN 1469-7580
YR 2019
FD 2019
LK http://riull.ull.es/xmlui/handle/915/35002
UL http://riull.ull.es/xmlui/handle/915/35002
LA en
DS Repositorio institucional de la Universidad de La Laguna
RD 14-jun-2024