XB-ART-10674J Neurophysiol July 1, 2000; 84 (1): 472-83.
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 depends on extracellular Ca(2+) 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 potentiation 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 Ca(2+) influx through voltage-gated Ca(2+) channels is not required. TrkB autophosphorylation is not blocked in Ca(2+)-free conditions, indicating that TrkB activity is not Ca(2+) dependent. Additionally, an inhibitor of phospholipase C interferes with BDNF-induced potentiation. These results suggest that activation of the TrkB receptor activates phospholipase C to initiate intracellular Ca(2+) release from stores which subsequently potentiates transmitter release.
PubMed ID: 10899220
PMC ID: PMC2710114
Article link: J Neurophysiol
Species referenced: Xenopus laevis
Genes referenced: bdnf ntrk2
References [+] :
Barish, Voltage-gated calcium currents in cultured embryonic Xenopus spinal neurones. 1992, Pubmed, Xenbase