title: Activation and response to axotomy of microglia in the facial motor nuclei of G93A superoxide dismutase transgenic mice.
abstract: Mice over-expressing a human mutation of Cu(2+)/Zn(2+) superoxide dismutase (SOD1) provide a model of amyotrophic lateral sclerosis. Using tomato lectin histochemistry, we analyzed microglia in the facial nuclei of SOD1(G93A) transgenic mice in the late stage of disease. In these animals, microglia was markedly activated, and ensheathed facial motoneurons as observed in wild-type mice 1 week after nerve transection. In the axotomized facial nucleus of transgenic mice at the same time point, microglia activation was enhanced and exhibited phagocytic features. The findings show that in the facial nucleus microglial cells react to motoneuron disease caused by the SOD1 mutation and to axotomy-induced damage of facial motoneurons.
authors.affiliation: Department of Morphological and Biomedical Sciences, Section of Anatomy and Histology, Medical Faculty, University of Verona, Strada Le Grazie 8, 37134, Verona, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Mariotti
authors.forename: M
authors.initials: M
authors.lastname: Bentivoglio
mesh_terms: D000409:Alanine / Q000235:genetics; D000690:Amyotrophic Lateral Sclerosis / Q000201:enzymology* / Q000235:genetics*; D000818:Animals; D019771:Axotomy; D004195:Disease Models, Animal; D005154:Facial Nerve / Q000201:enzymology / Q000502:physiology*; D005998:Glycine / Q000235:genetics; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D017628:Microglia / Q000201:enzymology / Q000502:physiology*; D009046:Motor Neurons / Q000201:enzymology / Q000502:physiology*; D013482:Superoxide Dismutase / Q000096:biosynthesis / Q000235:genetics*; D000072105:Superoxide Dismutase-1
chemical_list: C000606290:SOD1 protein, human; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D000409:Alanine; D005998:Glycine