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Retinoic acid delineates the topography of neuronal plasticity in postnatal cerebral cortex
Author(s) -
Wagner Elisabeth,
Luo Tuanlian,
Sakai Yasuo,
Parada Luis F.,
Dräger Ursula C.
Publication year - 2006
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.1460-9568.2006.04934.x
Subject(s) - retinoic acid , perineuronal net , biology , neuroscience , neocortex , cortex (anatomy) , cerebral cortex , parvalbumin , neural cell adhesion molecule , neuroplasticity , microbiology and biotechnology , biochemistry , cell , cell adhesion , gene
Retinoic acid is well recognized to promote neuronal differentiation in the embryonic nervous system, but how it influences the postnatal cerebral cortex remains largely unknown. The domain of highest retinoic acid actions in the cortex of the mouse constricts postnatally to a narrow band that includes the dorsal visual stream and the attentional and executive networks. This band of cortex, which is distinguished by the retinoic acid‐synthesizing enzyme RALDH3, exhibits signs of delayed maturation and enhanced plasticity compared to the surrounding cortex, as indicated by suppression of parvalbumin, neurofilament, cytochrome oxidase and perineuronal net maturation, and persistence of the embryonic, polysialated form of the neural cell‐adhesion molecule PSA‐NCAM. During the first postnatal week, the RALDH3‐expressing territory translocates in the caudal cortex from the medial limbic lobe to the adjacent neocortex. This topographical shift requires the neurotrophin NT‐3 because in mice lacking neuronal NT‐3 the RALDH3 enzyme maintains its early postnatal pattern up to adulthood. In the NT‐3‐null mutants, expression of the markers, whose topography colocalizes with RALDH3 in the normal cortex, matches the abnormal RALDH3 pattern. This indicates that the uneven retinoic acid distribution serves a role in patterning the maturation and to some extent function of the normal postnatal cerebral cortex.