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J Neurophysiol 84: 472-483, 2000;
0022-3077/00 $5.00
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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 472-483
Copyright ©2000 by the American Physiological Society

BDNF-Induced Potentiation of Spontaneous Twitching in Innervated Myocytes Requires Calcium Release From Intracellular Stores

Robin J. Kleiman,1 Ning Tian,2 David Krizaj,1 Thomas N. Hwang,1 David R. Copenhagen,1,2 and Louis F. Reichardt1,3

 1Department of Physiology,  2Department of Ophthalmology, and  3Howard Hughes Medical Institute, University of California, San Francisco, California 94143-0723

Kleiman, Robin J., Ning Tian, David Krizaj, Thomas N. Hwang, David R. Copenhagen, and Louis F. Reichardt. BDNF-Induced Potentiation of Spontaneous Twitching in Innervated Myocytes Requires Calcium Release From Intracellular Stores. J. Neurophysiol. 84: 472-483, 2000. Brain-derived neurotrophic factor (BDNF) can potentiate synaptic release at newly developed frog neuromuscular junctions. Although this potentiation depends 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 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 Ca2+ influx through voltage-gated Ca2+ channels is not required. TrkB autophosphorylation is not blocked in Ca2+-free conditions, indicating that TrkB activity is not Ca2+ 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 Ca2+ release from stores which subsequently potentiates transmitter release.




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