Neuronal death in the lateral geniculate nucleus of young ferrets following a cortical lesion: time-course, age dependence and involvement of caspases.

Détails

ID Serval
serval:BIB_3F734A423CCD
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Neuronal death in the lateral geniculate nucleus of young ferrets following a cortical lesion: time-course, age dependence and involvement of caspases.
Périodique
Brain Research
Auteur(s)
Gautschi M., Clarke P.G.
ISSN
0006-8993 (Print)
ISSN-L
0006-8993
Statut éditorial
Publié
Date de publication
2007
Peer-reviewed
Oui
Volume
1167
Pages
20-30
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
In humans and many other mammalian species, the behavioural consequences of a cortical lesion tend to be milder when it occurs early in life, and there is evidence that an important factor contributing to the behavioural sparing in the young is the formation of new thalamo-cortical connections by thalamic neurons initially connected with the lesioned area. However, this plasticity may be hindered by the secondary death of many of these neurons owing to the elimination by the primary lesion of their trophic support from the cortex. With the long-term aim of preventing this neuronal death, we have here characterised its timing in the lateral geniculate nucleus of ferrets following lesions of the visual cortex on postnatal days 5, 10, 20 or 35. After the earliest lesions (P5 or P10), this cell death began rapidly and occurred synchronously, being maximal at 48 h and declining to zero over the next few days. Following later lesions the cell death began more slowly and continued for longer. The dying neurons contained activated caspase-3 and fragmented DNA and their number 2 days after a P5 lesion was reduced by the broad-band caspase inhibitor z-VAD.fmk. These experiments open the way for a concerted effort to enhance adaptive plasticity by neuroprotection in the hours or days following a cortical lesion.
Mots-clé
Age Factors, Aging/physiology, Amino Acid Chloromethyl Ketones/pharmacology, Amino Acid Chloromethyl Ketones/therapeutic use, Animals, Brain Damage, Chronic/physiopathology, Caspase 3/metabolism, Caspase Inhibitors, Cell Death/drug effects, Cell Death/physiology, DNA Fragmentation/drug effects, Denervation, Enzyme Inhibitors/pharmacology, Enzyme Inhibitors/therapeutic use, Female, Ferrets, Geniculate Bodies/enzymology, Geniculate Bodies/growth & development, Male, Nerve Degeneration/drug therapy, Nerve Degeneration/enzymology, Neuronal Plasticity/physiology, Neuroprotective Agents/pharmacology, Neuroprotective Agents/therapeutic use, Time Factors, Visual Cortex/injuries, Visual Pathways/enzymology, Visual Pathways/growth & development
Pubmed
Web of science
Création de la notice
20/01/2008 18:49
Dernière modification de la notice
03/03/2018 16:25
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