BDNF-induced potentiation of spontaneous twitching in innervated myocytes requires calcium release from intracellular stores

Brain-derived neurotrophic factor (BDNF) can potentiate synaptic release at newly developed frog neuromuscular junctions. Although this potentiation d epends on extracellular Ca2+ and reflects changes in acetylcholine release, little is known about the intracellular transduction or calcium signaling pathways. We have developed a video assay for neurotrophin-induced potentia tion of myocyte twitching as a measure of potentiation of synaptic activity . We use this assay to show that BDNF-induced synaptic potentiation is not blocked by cadmium, indicating that Ca2+ influx through voltage-gated Ca2channels is not required. TrkB autophosphorylation is not blocked in Ca2+-f ree conditions, indicating that TrkB activity is not Ca2+ dependent. Additi onally, an inhibitor of phospholipase C interferes with BDNF-induced potent iation. These results suggest that activation of the TrkB receptor activate s phospholipase C to initiate intracellular Ca2+ release from stores which subsequently potentiates transmitter release.