Article révisé par les pairs
Résumé : Calbindin D28K, an intracellular calcium-binding protein, acts as Ca2+ buffering system in the cytoplasm. By means of this property, calbindin may protect neurons against large fluctuations in free intracellular Ca2+ and, hence, may prevent cell death. Although axotomy causes a massive influx of calcium into the lesioned neurons, resection of the hypoglossal nerve does not induce extensive neuronal cell death in rats. Even several weeks after axotomy, about 70% of the motoneurons survive despite permanent target deprivation. The mechanisms responsible for this remarkable survival rate are unknown. In this study, we have looked at the modification of calbindin immunoreactivity in axotomized hypoglossal motoneurons. In non-axotomized motoneurons, no calbindin is detectable by immunocytochemistry. Axotomy induced an increase of calbindin immunoreactivity in lesioned motoneurons. This increase, visualised by the number of calbindin-immunoreactive neurons extended from 1 day to 28 days. At this time most, but not all, motoneurons located on the side of the lesion were calbindin-positive as shown by retrograde labeling and immunoquenching. From 14 days post operation, calbindin immunoreactivity decreased and reached its basal value after 35 days post operation. At that time, only fibres were still calbindin immunoreactive. Interestingly, calbindin-immunoreactivity was also increased in almost all cell nuclei, compatible with a nuclear regulation. These data are consistent with the hypothesis that, as a reaction to axotomy, motoneurons trigger an increase in calbindin expression which acts as a compensatory Ca(2+)-buffering system, enabling neurons to maintain Ca2+ homeostasis and the survival of many motoneurons after axotomy.

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