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

Author

Listed:
  • 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)

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.

Suggested Citation

  • Christine R. Rose & Robert Blum & Bruno Pichler & Alexandra Lepier & Karl W. Kafitz & Arthur Konnerth, 2003. "Truncated TrkB-T1 mediates neurotrophin-evoked calcium signalling in glia cells," Nature, Nature, vol. 426(6962), pages 74-78, November.
    • Handle: RePEc:nat:nature:v:426:y:2003:i:6962:d:10.1038_nature01983
    DOI: 10.1038/nature01983
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