human BDNF-Biotin

Few examples in the literature emphasize the importance of using BDNF-biotin in living cells experiments. Pardridge, W.M. et al. demonstrated that the delivery of BDNF to the brain is non-existent owing to the combined effects of neglible blood brain barrier (BBB) transport and rapid systemic clearance1. The brain delivery of BDNF may be increased by conjugating biotinylated BDNF to BBB drug delivery vectors, such as neutral avidin conjugated to murine monoclonal antibody to the rat transferrin receptor1. Zhang, Y. and Pardridge, W.M. further showed that when BDNF is formulated to enable transport across the BBB, the intravenous administration of BDNF results in the reduction in stroke volume and improvement in functional outcome2. Du, J. et al. detected by using BDNF-biotin the ligand-induced TrkB internalization in cultured hippocampal neurons3. Bhattacharyya, A. et al. showed in mature sciatic nerves, that biotinylated BDNF activated Trk receptors function as rapid retrograde signal carriers to execute remote responses to target-derived neurotrophins4. Song, X.Y. et al. proved that exogenous BDNF-biotin is transported by the peripheral nerves following injection into the rat footpad and can be found in the sciatic nerves in fibres and vesicles5. Their data suggest that peripherally applied BDNF may have therapeutic effects on injured spinal cord. Xie, W. et al. followed the trafficking of QD-BDNF (Quantum Dot-BDNF) after its internalization at the axon terminal6. Their result showed that QD-BDNF could be used to track the movement of exogenous BDNF in neurons over long distances and to study the signaling organelles that contain BDNF6.