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.
