Consequence of parvalbumin deficiency in the mdx mouse: histological, biochemical and mechanical phenotype of a new double mutant
JM Raymackers, H Debaix, M Colson-Van Schoor… - Neuromuscular …, 2003 - Elsevier
We tested the hypothesis whether the mild dystrophy in mdx mice could result from the
contribution of the cytosolic calcium buffer parvalbumin in maintaining a normal cytosolic
[Ca2+] i, in spite of an increased passive Ca2+ influx. By crossing mdx mice with
parvalbumin-deficient mice, double mutant mice, lacking both dystrophin and parvalbumin,
were obtained. Though resting cytosolic [Ca2+] i and total calcium content were similar to
that of mdx muscles, this new animal model presented a slightly more severe phenotype …
contribution of the cytosolic calcium buffer parvalbumin in maintaining a normal cytosolic
[Ca2+] i, in spite of an increased passive Ca2+ influx. By crossing mdx mice with
parvalbumin-deficient mice, double mutant mice, lacking both dystrophin and parvalbumin,
were obtained. Though resting cytosolic [Ca2+] i and total calcium content were similar to
that of mdx muscles, this new animal model presented a slightly more severe phenotype …