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Volume 17, Number 18,
Issue of September 15, 1997
pp. 6918-6928
Copyright ©1997 Society for Neuroscience
Regulation of Mouse Skeletal Muscle L-Type Ca2+
Channel by Activation of the Insulin-Like Growth Factor-1 Receptor
Received March 27, 1997; revised June 30, 1997; accepted July 7, 1997.
Osvaldo Delbono1, 2,
Muthukrishnan Renganathan2, and
María Laura Messi 1
Departments of 1 Physiology and Pharmacology and
2 Internal Medicine (Gerontology), The Bowman Gray School of
Medicine of Wake Forest University, Winston-Salem, North Carolina 27157
We investigated the modulation of the skeletal muscle L-type
Ca2+ channel/dihydropyridine receptor in response to
insulin-like growth factor-1 receptor (IGF-1R) activation in single
extensor digitorum longus muscle fibers from adult C57BL/6 mice. The
L-type Ca2+ channel activity in its dual role as a
voltage sensor and a selective Ca2+-conducting pore
was recorded in voltage-clamp conditions. Peak Ca2+
current amplitude consistently increased after exposure to 20 ng/ml
IGF-1 (EC50 = 5.6 ± 1.8 nM). Peak IGF-1
effect on current amplitude at  20 mV was 210 ± 18% of the
control. Ca2+ current potentiation resulted from a
shift in 13 mV of the Ca2+ current-voltage
relationship toward more negative potentials. The IGF-1-induced
facilitation of the Ca2+ current was not associated
with an effect on charge movement amplitude and/or voltage
distribution. These phenomena suggest that the L-type
Ca2+ channel structures involved in voltage sensing
are not involved in the response to the growth factor. The modulatory
effect of IGF-1 on L-type Ca2+ channel was blocked
by tyrosine kinase and PKC inhibitors, but not by a cAMP-dependent
protein kinase inhibitor. IGF-1-dependent phosphorylation of the L-type
Ca2+ channel  1 subunit was demonstrated by
incorporation of [ -32P]ATP to monolayers of adult
fast-twitch skeletal muscles. IGF-1 induced phosphorylation of a
protein at the 165 kDa band, corresponding to the L-type
Ca2+ channel 1 subunit. These results
show that the activation of the IGF-1R facilitates skeletal muscle
L-type Ca2+ channel activity via a PKC-dependent
phosphorylation mechanism.
Key words:
insulin-like growth factor;
calcium channel;
skeletal
muscle;
muscle fiber;
phosphorylation
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