PubMed · 12053626
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Cornelius Woelk. 2002. Treating persistent cough: caution!. https://pubmed.ncbi.nlm.nih.gov/12053626/
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We tested the hypothesis that increased Ca2+ uptake in rat extensor digitorum longus (EDL) muscle elicits cell membrane damage as assessed from release of the intracellular enzyme lactate dehydrogenase (LDH). This was done by using 1) electrostimulation, 2) electroporation, and 3) the Ca2+ ionophore A23187. Stimulation at 1 Hz for 120-240 min caused an increase in 45Ca uptake that was closely correlated to LDH release. This LDH release increased markedly with temperature. After 120 min of stimulation at 1 Hz, resting 45Ca uptake was increased 5.6-fold compared with unstimulated muscles. This was associated with an eightfold increase in LDH release, and this effect was halved by lowering extracellular Ca2+ concentration ([Ca2+]o). The poststimulatory increase in resting 45Ca uptake persisted for at least 120 min. An acute increase in sarcolemma leakiness induced by electroporation markedly increased 45Ca uptake and LDH leakage. Both effects depended on [Ca2+]o. A23187 increased 45Ca uptake. Concomitantly, LDH leakage increased 18-fold within 30 min, and this effect was abolished by omitting Ca2+ from the buffer. We conclude that increased Ca2+ influx may be an important cause of cell membrane damage that arises during and after exercise or electrical shocks. Because membrane damage allows further influx of Ca2+, this results in positive feedback that may further increase membrane degeneration.
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The Drosophila Rel transcription factor Dorsal and its inhibitor Cactus participate in a signal transduction pathway involved in several biologic processes, including embryonic pattern formation, immunity, and muscle development. In contrast with embryonic muscle, where Dorsal is reportedly absent, this protein and Cactus accumulates in the neuromuscular junctions in the muscle of both larvae and adults. The phenotype of homozygous dorsal mutant larvae suggested that Dorsal and Cactus maybe necessary for normal function and maintenance of the neuromuscular system. Here we investigate if these proteins can respond to synaptic activity. Using larval body wall preparations and antibodies specific for Dorsal or Cactus we show that the amount of these proteins at the neuromuscular junction is substantially decreased after electrical stimulation of the nerves or incubation in glutamate, the principal transmitter in this type of synapse. The specificity of the response was tested with a glutamate receptor antagonist (argiotoxin 636). Because the effect can be reproduced using a calcium ionophore (ionomycin treatment) as well as blocked by the inhibition of the muscle ryanodine receptor (tetracaine treatment), the involvement of calcium in this process seems likely. We also observed that the inhibition of the calcium dependent protein phosphatase calcineurin prevents the effect of glutamate on the fluorescence for Dorsal and Cactus, suggesting its participation in a signal transduction cascade that may activate Dorsal in the muscle independently of Toll. Our results are consistent with a novel function of the Rel factor Dorsal in a molecular pathway turned on by neural activity and/or contractile activity.