Titre
Modulation of the gap junction protein Connexin36 in neurons in a mouse model of transient focalcerebral ischemia
Type
mémoire de master/maîtrise/licence
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Auteur(s)
Handschin, L.
Auteure/Auteur
Directrices/directeurs
Haefliger, J.-A.
Directeur⸱rice
Hirt, L.
Codirecteur⸱rice
Liens vers les personnes
Liens vers les unités
Faculté
Université de Lausanne, Faculté de biologie et médecine
Statut éditorial
Accepté
Date de publication
2011
Nombre de pages
26
Langue
anglais
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.
Sujets
PID Serval
serval:BIB_270B5D8787C1
Date de création
2012-06-05T09:24:35.337Z
Date de création dans IRIS
2025-05-20T16:26:20Z
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Nom
BIB_270B5D8787C1.P001.pdf
Version du manuscrit
imprimatur
Taille
2.14 MB
Format
Adobe PDF
PID Serval
serval:BIB_270B5D8787C1.P001
URN
urn:nbn:ch:serval-BIB_270B5D8787C10
Somme de contrôle
(MD5):0a286dff552e8c036f0f55ba61dc7d6e