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The coupling of a trkB tyrosine residue to LTP
Patrik Ernfors1, Clive R Bramham
1Unit of Molecular Neurobiology, MBB, Karolinska Institute, S-171 77 Stockholm, Sweden. patrik.ernfors@mbb.ki.se
Trends in Neurosciences
|April 12, 2003
Abstract:
Brain-derived neurotrophic factor (BDNF) and its receptor, trkB, activate cAMP-response-element-binding protein (CREB) and the transcription of genes that is crucial for long-term potentiation (LTP). Any of several signaling pathways activated by trkB could be required for LTP. A recent study using mice carrying a mutation in a specific tyrosine residue of trkB pinpoints a necessary role for the phospholipase-Cgamma (PLCgamma) pathway in CREB activation and LTP maintenance.