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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 472-483
Copyright ©2000 by the American Physiological Society
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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