Truncated TrkB-T1 mediates neurotrophin-evoked calcium signalling in glia cells

Christine R. Rose (), Robert Blum, Bruno Pichler, Alexandra Lepier, Karl W. Kafitz and Arthur Konnerth ()
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Christine R. Rose: Ludwig-Maximilians-Universität München
Robert Blum: Ludwig-Maximilians-Universität München
Bruno Pichler: Ludwig-Maximilians-Universität München
Alexandra Lepier: Ludwig-Maximilians-Universität München
Karl W. Kafitz: Ludwig-Maximilians-Universität München
Arthur Konnerth: Ludwig-Maximilians-Universität München

Nature, 2003, vol. 426, issue 6962, 74-78

Abstract: Abstract The neurotrophin receptor TrkB is essential for normal function of the mammalian brain1,2,3. It is expressed in three splice variants. Full-length receptors (TrkBFL) possess an intracellular tyrosine kinase domain and are considered as those TrkB receptors that mediate the crucial effects of brain-derived neurotrophic factor (BDNF) or neurotrophin 4/5 (NT-4/5). By contrast, truncated receptors (TrkB-T1 and TrkB-T2) lack tyrosine kinase activity and have not been reported to elicit rapid intracellular signalling4. Here we show that astrocytes predominately express TrkB-T1 and respond to brief application of BDNF by releasing calcium from intracellular stores. The calcium transients are insensitive to the tyrosine kinase blocker K-252a and persist in mutant mice lacking TrkBFL. By contrast, neurons produce rapid BDNF-evoked signals through TrkBFL and the Nav1.9 channel5,6. Expression of antisense TrkB messenger RNA strongly reduces BDNF-evoked calcium signals in glia. Thus, our results show that, unexpectedly, TrkB-T1 has a direct signalling role in mediating inositol-1,4,5-trisphosphate-dependent calcium release; in addition, they identify a previously unknown mechanism of neurotrophin action in the brain.

Date: 2003
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DOI: 10.1038/nature01983

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