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Published online 13 December 2004. doi:10.1083/jcb.200404106
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 6, 1205-1215
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Article

BDNF-induced recruitment of TrkB receptor into neuronal lipid rafts

: roles in synaptic modulation



Shingo Suzuki1,2,3, Tadahiro Numakawa4, Kazuhiro Shimazu6, Hisatsugu Koshimizu1, Tomoko Hara1, Hiroshi Hatanaka2, Lin Mei5, Bai Lu6, and Masami Kojima1,3

1 Research Institute for Cell Engineering, National Institute of Advanced Industrial Science and Technology (AIST), Ikeda, Osaka, 563-8577, Japan
2 Institute for Protein Research, Osaka University, Suita, Osaka, 565-0871, Japan
3 Solution Oriented Research for Science and Technology, Japan Science and Technology Agency, Kawaguchi, Saitama, 332-0012, Japan
4 National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, 187-8502, Japan
5 Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, GA 30912
6 Section on Neural Development and Plasticity, NICHD, National Institutes of Health, Bethesda, MD 20892

Correspondence to Masami Kojima: m-kojima{at}aist.go.jp; or Bai Lu: bailu{at}mail.NIH.gov

Brain-derived neurotrophic factor (BDNF) plays an important role in synaptic plasticity but the underlying signaling mechanisms remain unknown. Here, we show that BDNF rapidly recruits full-length TrkB (TrkB-FL) receptor into cholesterol-rich lipid rafts from nonraft regions of neuronal plasma membranes. Translocation of TrkB-FL was blocked by Trk inhibitors, suggesting a role of TrkB tyrosine kinase in the translocation. Disruption of lipid rafts by depleting cholesterol from cell surface blocked the ligand-induced translocation. Moreover, disruption of lipid rafts prevented potentiating effects of BDNF on transmitter release in cultured neurons and synaptic response to tetanus in hippocampal slices. In contrast, lipid rafts are not required for BDNF regulation of neuronal survival. Thus, ligand-induced TrkB translocation into lipid rafts may represent a signaling mechanism selective for synaptic modulation by BDNF in the central nervous system.

Abbreviations used in this paper: 4-AP, 4-amino pyridine; BDNF, brain-derived neurotrophic factor; CNS, central nervous system; GDNF, glial cell line–derived neurotrophic factor; GPI, glycosylphosphatidylinositol; HFS, high frequency stimulation; KRH, Krebs'-Ringer's-Henseleit; LTP, long-term potentiation; MCD, methyl-ß-cyclodextrin; PI3-K, phosphatidylinositol 3-kinase; RTK, receptor tyrosine kinase; TrkB-FL, full-length TrkB.


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