Relevance of exocytotic glutamate release from retinal glia.


  • Slezak Michal
  • Grosche Antje
  • Niemiec Aurore
  • Tanimoto Naoyuki
  • Pannicke Thomas
  • Münch Thomas A
  • Crocker Britni
  • Isope Philippe
  • Härtig Wolfgang
  • Beck Susanne C
  • Huber Gesine
  • Ferracci Geraldine
  • Perraut Martine
  • Reber Michael
  • Miehe Monique
  • Demais Valérie
  • Lévêque Christian
  • Metzger Daniel
  • Szklarczyk Klaudia
  • Przewlocki Ryszard
  • Seeliger Mathias W
  • Sage-Ciocca Dominique
  • Hirrlinger Johannes
  • Reichenbach Andreas
  • Reibel Sophie
  • Pfrieger Frank W


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 Müller 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.

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