Fig. 8.

Schematic diagrams showing the two models for the blocking action of BDNF on LTD. In A, BDNF is hypothesized to be derived from presynaptic sites and to serve as an inhibitor for an LTD expression factor that would be released from postsynaptic sites. In this model, LFS is supposed to induce a mild level of depolarization and a consequent rise of Ca²⁺ in postsynaptic sites through activation of glutamate receptors (Glu-R) and voltage-dependent Ca²⁺ channels (VDCC). This rise of Ca²⁺ would activate an unknown process, which in turn would release or produce the LTD expression factor. This factor would decrease transmitter release from presynaptic terminals for a long time. The activation of TrkB by BDNF would then suppress the action of this factor in presynaptic terminals. In B, BDNF itself is hypothesized to operate as an LTD-blocking or a synaptic transmission-maintaining factor. The LFS-induced rise in postsynaptic Ca²⁺ would activate an unknown factor, possibly protein phosphatases, which would suppress the release or production of BDNF at postsynaptic sites. This would in turn lead to a shortage of BDNF at presynaptic terminals. Thus, LFS without support of BDNF would lead to a decrease in transmitter release from presynaptic terminals for a long time.