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Transient maternal hypothyroxinemia at onset of corticogenesis alters tangential migration of medial ganglionic eminence‐derived neurons
Author(s) -
Cuevas Estela,
Ausó Eva,
Telefont Martin,
De Escobar Gabriella Morreale,
Sotelo Constantino,
Berbel Pere
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.04243.x
Subject(s) - ganglionic eminence , corticogenesis , biology , neocortex , cerebral cortex , neuroscience , green fluorescent protein , cortex (anatomy) , anatomy , embryo , neuronal migration , microbiology and biotechnology , central nervous system , cerebrum , genetics , progenitor cell , gene , stem cell
Correct positioning of cortical neurons during development depends on the radial migration of the projection neurons and on the coordinated tangential and radial migrations of the subcortically generated interneurons. As previously shown, a transient and moderate maternal deficiency in thyroxin during early corticogenesis alters the radial migration of projection neurons. To determine if a similar effect might also affect tangential migration of medial ganglionic eminence (MGE)‐derived neurons at the origin of cortical interneurons, explants of MGE from green fluorescent protein (GFP)‐transgenic embryos were implanted into flat cortical mounts from wild‐type embryos. The distances covered and the preferential migration (medially) of GFP‐MGE neurons from embryos of hypothyroxinemic dams are not affected in their tangential migration into wild‐type control cortices. In contrast, when GFP‐MGE neurons from embryos of control or hypothyroxinemic dams migrate within cortices from embryos of hypothyroxinemic dams, the GFP‐MGE‐derived neurons lose their preferential direction of migration, although they still migrate for long distances throughout the cortex. Our results show that maternal hypothyroxinemia alters the tangential migration of GFP‐MGE‐derived neurons in the neocortex of the progeny and suggest that this alteration is not derived from the migratory neurons themselves but through undefined short‐ and long‐range cues responsible for the guidance of their migration.