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. 2006 Dec 27;26(52):13531–13536. doi: 10.1523/JNEUROSCI.4576-06.2006

Figure 3.

Figure 3.

Summary of the different manipulations on the presynaptic action of released BDNF. A, Plot of average event frequency at 22–27 min during the recordings normalized to baseline. K252a (Bath), anti-BDNF, and Box2+3 were significantly different from Box1 (p < 0.01, two-tailed Student's t test), whereas BDNF and K252a (Int) were not (p > 0.3 and p > 0.6, respectively, two-tailed Student's t test). B, Diagrammatic summary of the proposed mechanism by which postsynaptic depolarization leads to an increase in presynaptic transmitter release. Postsynaptic depolarization evokes calcium-dependent release of BDNF from dendrites (1). BDNF diffuses retrogradely from the postsynaptic to the presynaptic terminals (2) and activates presynaptic trkB receptors (3). This in turn elicits an increase in vesicle release probability (4). These steps were confirmed by interrupting regulated release, with a BDNF scavenging antibody to block diffusion and by blocking presynaptic trkB function. Error bars indicate ± SEM. NT vesicle, Neurotransmitter-containing vesicle.