Key result
In adult mdx mice, resting cytosolic Ca2+ was not chronically elevated compared to controls, while parvalbumin expression increased threefold in fast muscles, potentially maintaining normal Ca2+ levels.
Population
Adult mdx mouse (animal model of Duchenne muscular dystrophy) and control mice
Design
Review
Authors
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Challenges Ca2+ elevation hypothesis in mdx models; leaves open compensatory parvalbumin mechanisms for DMD research.
The study challenges the hypothesis of chronically elevated cytosolic calcium in mdx mice, suggesting that increased parvalbumin expression may help maintain normal calcium levels.
Jean‐Marie Gillis (1996) conducted a review in Duchenne muscular dystrophy (mdx mouse model). mdx mutation (dystrophin deficiency) vs. control mice was evaluated on Resting intracellular calcium concentration ([Ca2+]i) and parvalbumin expression. In adult mdx mice, resting cytosolic Ca2+ was not chronically elevated compared to controls, while parvalbumin expression increased threefold in fast muscles, potentially maintaining normal Ca2+ levels.