Fast retrograde effects on neuronal death and dendritic organization in development: the role of calcium influx.

Détails

ID Serval
serval:BIB_448145EE820A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Fast retrograde effects on neuronal death and dendritic organization in development: the role of calcium influx.
Périodique
Neuroscience
Auteur(s)
Posada A., Clarke P.G.H.
ISSN
0306-4522[print], 0306-4522[linking]
Statut éditorial
Publié
Date de publication
1999
Volume
89
Numéro
2
Pages
399-408
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: ppublish
Résumé
Retrograde signals from axon terminal to cell body are known to regulate neuronal survival and differentiation during development. They are generally attributed to the uptake and transport of trophic factors, but there is recent evidence in the isthmo-optic nucleus for a remarkably fast-acting retrograde signal from the contralateral retina that is not mediated by the conventional trophic route. The isthmo-optic nucleus undergoes 55% neuron death between embryonic days 12 and 17, and becomes laminated at embryonic day 14 owing to dendritic re-organization. Blockade of retinal electrical activity just before day 14 reduces neuronal death and lamination in the isthmo-optic nucleus within as little as 6 h. We here investigate how action potentials initiate the fast-acting retrograde signal, and we provide evidence that the first step is calcium entry into the isthmo-optic axon terminals. Neuronal death and lamination are rapidly reduced in the isthmo-optic nucleus by intraocularly injected omega-conotoxin, a blocker of N-type calcium channels known to be located mainly on axon terminal. Similar effects occurred with two other calcium channel blockers (cadmium and alpha-bungarotoxin) believed to act on both the isthmo-optic terminals and their target cells, but not with nifedipine, a blocker of L-type (mainly somatic) channels, supporting a presynaptic initiation of the fast signal. Nevertheless postsynaptic events may also be involved because pharmacological destruction of the amacrine targets cells of the isthmo-optic nucleus reduced its cell death and lamination 9-12 h later.
Mots-clé
Animals, Brain/drug effects, Brain/embryology, Bungarotoxins/pharmacology, Calcium/metabolism, Calcium Channel Blockers/pharmacology, Calcium Channels/drug effects, Calcium Channels/physiology, Cell Death/physiology, Chick Embryo, Dendrites/physiology, Electrophysiology, Embryo, Mammalian/cytology, Embryo, Mammalian/drug effects, Embryo, Nonmammalian, Neurons/physiology, Nicotinic Antagonists/pharmacology, Retina/drug effects, Signal Transduction/physiology, Time Factors, Visual Pathways/drug effects, Visual Pathways/embryology
Pubmed
Web of science
Création de la notice
20/01/2008 18:49
Dernière modification de la notice
20/08/2019 14:48
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