Relevance of exocytotic glutamate release from retinal glia.
Fiche publication
Date publication
mai 2012
Auteurs
Membres identifiés du Cancéropôle Est :
Dr METZGER Daniel, Mme DEMAIS Valérie, Dr PFRIEGER Frank
Tous les auteurs :
Slezak M, Grosche A, Niemiec A, Tanimoto N, Pannicke T, Munch TA, Crocker B, Isope P, Hartig W, Beck SC, Huber G, Ferracci G, Perraut M, Reber M, Miehe M, Demais V, Leveque C, Metzger D, Szklarczyk K, Przewlocki R, Seeliger MW, Sage-Ciocca D, Hirrlinger J, Reichenbach A, Reibel S, Pfrieger FW
Lien Pubmed
Résumé
Glial cells release molecules that influence brain development, function, and disease. Calcium-dependent exocytosis has been proposed as potential release mechanism in astroglia, but the physiological relevance of "gliotransmission" in vivo remains controversial. We focused on the impact of glial exocytosis on sensory transduction in the retina. To this end, we generated transgenic mice to block exocytosis by Cre recombinase-dependent expression of the clostridial botulinum neurotoxin serotype B light chain, which cleaves vesicle-associated membrane protein 1-3. Ubiquitous and neuronal toxin expression caused perinatal lethality and a reduction of synaptic transmission thus validating transgene function. Toxin expression in Muller cells inhibited vesicular glutamate release and impaired glial volume regulation but left retinal histology and visual processing unaffected. Our model to study gliotransmission in vivo reveals specific functions of exocytotic glutamate release in retinal glia.
Référence
Neuron. 2012 May 10;74(3):504-16.