title: Changes in the expression of P2X1 and P2X2 purinergic receptors in facial motoneurons after nerve lesions in rodents and correlation with motoneuron degeneration.
abstract: Involvement of P2X1 and P2X2 purinergic receptors in motoneuron response to injury was investigated with Western blotting and immunohistochemistry and correlated with motoneuron loss, Bcl-2 expression, nitric oxide synthase induction and glial activation. P2X1 was highly induced in rat facial motoneurons after nerve resection, which causes slowly occurring neurodegeneration. P2X1 induction was lower and less persistent after nerve crush, permissive for fiber regeneration. P2X2 expression was found in nuclei of rat facial motoneurons, with nuclear export in the cytoplasm after nerve resection. P2X1 induction in axotomized facial motoneurons was impaired in superoxide dismutase (SOD)1-G93A-mutant mice, a model of motoneuron disease. The data in rats point to a correlation of P2X1 induction with motoneuron degeneration, which also involves P2X2 intracellular changes, rather than with axon regeneration effort. The data in mice show that the SOD1 mutation interferes with injury-elicited P2X1 induction, suggesting alterations of ATP release from mutant motoneurons after damage.
authors.affiliation: Department of Morphological and Biomedical Sciences, Faculty of Medicine, Strada Le Grazie 8, 37134 Verona, Italy.
authors.forename: Roman M
authors.initials: RM
authors.lastname: Kassa
authors.forename: Marina
authors.initials: M
authors.lastname: Bentivoglio
authors.forename: Raffaella
authors.initials: R
authors.lastname: Mariotti
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002452:Cell Count; D004790:Enzyme Induction / Q000187:drug effects; D005152:Facial Muscles / Q000294:innervation* / Q000473:pathology*; D005154:Facial Nerve / Q000473:pathology* / Q000502:physiology*; D005455:Fluorescent Antibody Technique; D007150:Immunohistochemistry; D008297:Male; D016472:Motor Neuron Disease / Q000473:pathology*; D009046:Motor Neurons / Q000378:metabolism* / Q000473:pathology*; D009154:Mutation / Q000502:physiology; D009252:NADPH Dehydrogenase / Q000378:metabolism; D009409:Nerve Crush; D009410:Nerve Degeneration / Q000473:pathology*; D009457:Neuroglia / Q000187:drug effects; D052248:Nitric Oxide Synthase Type I / Q000096:biosynthesis; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018048:Receptors, Purinergic P2 / Q000096:biosynthesis*; D058469:Receptors, Purinergic P2X; D058476:Receptors, Purinergic P2X2; D013482:Superoxide Dismutase / Q000235:genetics; D000072105:Superoxide Dismutase-1
chemical_list: C546402:P2rx2 protein, mouse; C546403:P2rx2 protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; D018048:Receptors, Purinergic P2; D058469:Receptors, Purinergic P2X; D058476:Receptors, Purinergic P2X2; D052248:Nitric Oxide Synthase Type I; C000606291:Sod1 protein, mouse; C000606292:Sod1 protein, rat; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D009252:NADPH Dehydrogenase