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Volume 17, Number 3,
Issue of February 1, 1997
pp. 904-916
Copyright ©1997 Society for Neuroscience
Kinetics, Ca2+ Dependence, and Biophysical Properties
of Integrin-Mediated Mechanical Modulation of Transmitter Release from
Frog Motor Nerve Terminals
Received Sept. 20, 1996; revised Nov. 7, 1996; accepted Nov. 11, 1996.
Bo-Ming Chen and
Alan D. Grinnell
Department of Physiology, Jerry Lewis Neuromuscular Research
Center, and Ahmanson Laboratory of Neurobiology, University of
California Los Angeles School of Medicine, Los Angeles, California
90095
Neurotransmitter release from frog motor nerve terminals is
strongly modulated by change in muscle length. Over the physiological range, there is an ~10% increase in spontaneous and evoked release per 1% muscle stretch. Because many muscle fibers do not receive suprathreshold synaptic inputs at rest length, this stretch-induced enhancement of release constitutes a strong peripheral amplifier of the
spinal stretch reflex. The stretch modulation of release is inhibited
by peptides that block integrin binding of natural ligands. The
modulation varies linearly with length, with a delay of no more than
~1-2 msec and is maintained constant at the new length. Moreover, the
stretch modulation persists in a zero Ca2+ Ringer and,
hence, is not dependent on Ca2+ influx through stretch
activated channels. Eliminating transmembrane Ca2+
gradients and buffering intraterminal Ca2+ to approximately
normal resting levels does not eliminate the modulation, suggesting
that it is not the result of release of Ca2+ from internal
stores. Finally, changes in temperature have no detectable effect on
the kinetics of stretch-induced changes in endplate potential (EPP)
amplitude or miniature EPP (mEPP) frequency. We conclude, therefore,
that stretch does not act via second messenger pathways or a chemical
modification of molecules involved in the release pathway. Instead,
there is direct mechanical modulation of release. We postulate that
tension on integrins in the presynaptic membrane is transduced
mechanically into changes in the position or conformation of one or
more molecules involved in neurotransmitter release, altering
sensitivity to Ca2+ or the equilibrium for a critical
reaction leading to vesicle fusion.
Key words:
synaptic plasticity;
EPPs;
mEPPs;
muscle length;
neuromuscular junction;
mechanotransduction;
RGD;
muscle stretch
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