par Dassesse, Donald 
;Cuvelier, Laetitia ;Krebs, Claudia;Streppel, Michael;Guntinas-Lichius, Orlando;Neiss, Wolfram F.;Pochet, Roland
Référence Brain research, 786, 1-2, page (181-188)
Publication Publié, 1998-03
;Cuvelier, Laetitia ;Krebs, Claudia;Streppel, Michael;Guntinas-Lichius, Orlando;Neiss, Wolfram F.;Pochet, Roland Référence Brain research, 786, 1-2, page (181-188)
Publication Publié, 1998-03
Article révisé par les pairs
| Résumé : | Axotomy induces a profound modification of Ca2+ homeostasis in injured neurons which may lead to neuronal death. Remarkably, after axotomy and resection of the hypoglossal nerve, 65-75% of the hypoglossal motoneurons survive in the long term and this suggests some adaptive mechanisms compensating the massive calcium influx. As potential components of this adaptation, we have examined calmodulin and calbindin-D28k by in situ hybridisation and immunohistochemistry in motoneurons of the rat after hypoglossal nerve transection. Neuronal calbindin mRNA and protein content was low in normal state, transiently increased to 200% of the basal expression at 8 days post-operation (dpo), then declined to normal again until 28 dpo. Calmodulin mRNA was highly expressed in normal hypoglossal motoneurons and remained constant after axotomy. Calmodulin protein immunoreactivity, however, was transiently decreased in axotomised motoneurons suggesting post-transcriptional modification. The upregulation of calbindin expression may facilitate the survival of injured motoneurons. |
