Modulation of the gap junction protein Connexin36 in neurons in a mouse model of transient focalcerebral ischemia

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Ressource 1Télécharger: BIB_270B5D8787C1.P001.pdf (2189.44 [Ko])
Etat: Public
Version: Après imprimatur
ID Serval
serval:BIB_270B5D8787C1
Type
Mémoire
Sous-type
(Mémoire de) maîtrise (master)
Collection
Publications
Institution
Titre
Modulation of the gap junction protein Connexin36 in neurons in a mouse model of transient focalcerebral ischemia
Auteur(s)
Handschin L.
Directeur(s)
Haefliger J.-A.
Codirecteur(s)
Hirt L.
Détails de l'institution
Université de Lausanne, Faculté de biologie et médecine
Statut éditorial
Acceptée
Date de publication
2011
Langue
anglais
Nombre de pages
26
Résumé
Intercellular communication is achieved at specialized regions of the plasma membrane by¦gap junctions. Gap junctions are transmembrane channels allowing direct contacts between¦the cytoplasms of neighboring cells. Each cell participates with one hemichannel, or¦connexon, made of six protein subunits named connexins. Thanks to these junctions, cells¦potentially share a pool of small molecules and metabolites, such as nucleotides, amino acids¦and second messengers.¦In an ischemic (i.e. non-perfused) territory of the brain, irreversible damage progresses over¦time from the centre of the most severe flow reduction to the periphery with less disturbed¦perfusion. Functionally impaired tissue can survive and recover if sufficient reperfusion is reestablished¦within a limited time period, which depends on various factors and mechanisms¦modulating the signaling pathways leading to cell death.¦Observations were made indicating the presence of electrical coupling between neurons which¦resist better to an ischemic insult. This electrical coupling is likely to be mediated by¦Connexin36 (Cx36), a neuron specific connexin isoform. It was demonstrated in the past that¦global ischemia induces a selective upregulation of Cx36 expression in regions with neurons¦that survive the insult whereas others undergo apoptosis and die. These observations raise the¦possibility that the neuronal gap junction Cx36 might play a role in the destiny of neurons¦after cerebral ischemia.¦The aim of this work was to characterize the regulation of Connexin36 in a mouse model of¦transient focal cerebral ischemia by immunofluorescence and Western blot analysis. Our¦immunofluorescence results suggest a specific increase in Cx36 in the penumbral region of¦the ischemic hemisphere.
Mots-clé
Intercellular communication, Connexin, Cerebral ischemia
Création de la notice
05/06/2012 11:24
Dernière modification de la notice
20/08/2019 14:05
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