Abstract
We measured free intracellular calcium ([Ca 2+] i) in cultured cerebellar cells from normal and mdx mice. Resting levels of ([Ca 2+] i) were 24% higher in the dystrophic neurons ( normal: 61.2 ± 1.5nM calcium, n = 104; dystrophic: 76.1 ± 2.4nM calcium, n = 136, P < 0.01). Distrophic neurons showed a significantly greater increase in ([Ca 2+] i) in the presence of elevated (18 mM) extracellular calcium levels. Resting sodium levels ([Na +] i), however, were found to be similar in normal and dystrophic granule neurons. In addition, sodium influx rates after ouabain inhibition of the Na +/K + ATPase were also identical. Therefore, the increased permeability of granule neurons was specific to calcium, and did not result from a non-selective cation-permeable conductance. Unlike granule cells, astrocytes do not express dystrophin. Glial cells from normal and dystrophic mice showed no difference in their resting free calcium levels or their response to a high calcium load. Thus, cerebellar granule neurons from mdx mice show a calcium-specific regulatory defect similar to that found in dystrophic muscle fibers 15,47,48, while cerebellar glial cells, which do not normally express dystrophin, have no such defect.
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