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

Christine R. Rose, Robert Blum, Bruno Pichler, Alexandra Lepier, Karl W. Kafitz, Arthur Konnerth

Publikation: Beitrag in FachzeitschriftArtikelBegutachtung

310 Zitate (Scopus)

Abstract

The neurotrophin receptor TrkB is essential for normal function of the mammalian brain. 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 signalling. 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 TrkBFLand the Nav1.9 channel. 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.

OriginalspracheEnglisch
Seiten (von - bis)74-78
Seitenumfang5
FachzeitschriftNature
Jahrgang426
Ausgabenummer6962
DOIs
PublikationsstatusVeröffentlicht - 6 Nov. 2003
Extern publiziertJa

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