Dopamine affects parvalbumin expression during cortical development in vitro.

Détails

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Etat: Public
Version: Final published version
ID Serval
serval:BIB_FEF3F78789C1
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Dopamine affects parvalbumin expression during cortical development in vitro.
Périodique
The Journal of neuroscience : the official journal of the Society for Neuroscience
Auteur(s)
Porter L.L., Rizzo E., Hornung J.P.
ISSN
1529-2401 (Electronic)
ISSN-L
0270-6474
Statut éditorial
Publié
Date de publication
15/10/1999
Peer-reviewed
Oui
Volume
19
Numéro
20
Pages
8990-9003
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
Publication Status: ppublish
Résumé
This study was undertaken to determine how dopamine influences cortical development. It focused on morphogenesis of GABAergic neurons that contained the calcium-binding protein parvalbumin (PV). Organotypic slices of frontoparietal cortex were taken from neonatal rats, cultured with or without dopamine, harvested daily (4-30 d), and immunostained for parvalbumin. Expression of parvalbumin occurred in the same regional and laminar sequence as in vivo. Expression in cingulate and entorhinal preceded that in lateral frontoparietal cortices. Laminar expression progressed from layer V to VI and finally II-IV. Somal labeling preceded fiber labeling by 2 d. Dopamine accelerated PV expression. In treated slices, a dense band of PV-immunoreactive neurons appeared in layer V at 7 d in vitro (DIV), and in all layers of frontoparietal cortex at 14 DIV, whereas in control slices such labeling did not appear until 14 and 21 DIV, respectively. The laminar distribution and dendritic branching of PV-immunoreactive neurons were quantified. More labeled neurons were in the superficial layers, and their dendritic arborizations were significantly increased by dopamine. Treatment with a D1 receptor agonist had little effect, whereas a D2 agonist mimicked dopamine's effects. Likewise, the D2 but not the D1 antagonist blocked dopamine-induced changes, indicating that they were mediated primarily by D2 receptors. Parvalbumin expression was accelerated by dopaminergic reinnervation of cortical slices that were cocultured with mesencephalic slices. Coapplication of the glutamate NMDA receptor antagonist MK801 or AP5 blocked dopamine-induced increases in dendritic branching, suggesting that changes were mediated partly by interaction with glutamate to alter cortical excitability.

Mots-clé
Aging/metabolism, Animals, Animals, Newborn, Cerebral Cortex/cytology, Cerebral Cortex/drug effects, Cerebral Cortex/growth & development, Cerebral Cortex/metabolism, Dopamine/pharmacology, Dopamine/physiology, Glutamic Acid/physiology, In Vitro Techniques, Nerve Fibers/physiology, Neurons/metabolism, Parvalbumins/metabolism, Rats, Receptors, Dopamine D1/physiology, Receptors, Dopamine D2/physiology
Pubmed
Création de la notice
24/01/2008 15:22
Dernière modification de la notice
20/08/2019 17:29
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