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Updated: Aug 25, 2026

Ex Vivo Imaging of Cell-specific Calcium Signaling at the Tripartite Synapse of the Mouse Diaphragm
Published on: October 4, 2018
Activation of P-type calcium channel regulates a unique thapsigargin-sensitive calcium pool in embryonic motoneurons
Frédérique Scamps1, Anne Roig, Hassan Boukhaddaoui
1Inserm U-583, Université Montpellier II, Place Eugène Bataillon, Case 089, 34095, Montpellier, Cedex 5, France.
Abstract:
By regulating voltage-dependent Ca2+ influx and intracellular Ca2+ homeostasis, electrical activity plays a central role in motoneuron development. Dissociated cultures of purified embryonic rat motoneurons were used to explore the molecular mechanisms by which Ca2+ influx control [Ca2+]i transients in these neurons. Thapsigargin (250 nm) and cyclopiazonic acid (10 micro m), which deplete Ca2+ stores in the endoplasmic reticulum, decrease by 30% the depolarization-induced [Ca2+]i transients in motoneurons without affecting voltage-activated calcium currents. This thapsigargin-sensitive intracellular Ca2+ pool differs from other previous described Ca2+ stores that are sensitive to ryanodine or caffeine, inositol triphosphate, insulin and from mitochondrial Ca2+ pools. Thapsigargin affected the Cav2.1 P-type Ca2+ channel component of the depolarization-induced [Ca2+]i transient in motoneurons but spared [Ca2+]i transient induced by Cav1 L-type and Cav2.2 N-type Ca2+ channel components, suggesting a close functional relationship between Cav2.1 subunit and this unique thapsigargin-sensitive Ca2+ store. Altogether the present results demonstrate a new pathway, used by embryonic motoneurons, to regulate Ca2+ signalling through voltage-activated (Cav2.1) Ca2+ channels.
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