Artículos de revistas
Progesterone treatment reduces NADPH-diaphorase/Nitric oxide synthase in Wobbler mouse motoneuron disease
Fecha
2004-12Registro en:
Gonzalez Deniselle, Maria Claudia; Garay, Laura Ines; López, Juan José; Gonzalez, Susana Laura; Mougel, Analía; et al.; Progesterone treatment reduces NADPH-diaphorase/Nitric oxide synthase in Wobbler mouse motoneuron disease; Elsevier Science; Brain Research; 1014; 1-2; 12-2004; 71-79
0006-8993
1872-6240
CONICET Digital
CONICET
Autor
Gonzalez Deniselle, Maria Claudia
Garay, Laura Ines
López, Juan José
Gonzalez, Susana Laura
Mougel, Analía
Guennoun, Rachida
Schumacher, Michael
de Nicola, Alejandro Federico
Resumen
Previous work demonstrated that progesterone (PROG) treatment attenuates morphological, molecular and functional abnormalities in the spinal cord of the Wobbler (Wr) mouse, a genetic model of motoneuron degeneration. Wr mice show a marked up-regulation of the nitric oxide synthesizing enzyme (NOS). Since nitric oxide is a highly reactive species, it may play a role in neuropathology of Wr mice. We now studied if PROG neuroprotection involved changes of NOS activity in motoneurons and astrocytes, determined by the nicotinamide adenine dinucleotide phosphate-diaphorase (NADPHD) histochemical reaction. Two and four-month-old Wr mice at the progressive and stabilization stages of the disease, respectively, and their age-matched controls were left untreated or received a single 20-mg PROG pellet for 18 days. PROG reduced the high number of NADPHD-active motoneurons and white matter astrocytes in 2-month-old Wr mice but was unable to change the low number of NADPHD-active motoneurons in 4-month-old Wr mice or astrocytes in this age group. A large number of motoneurons in 2-month-old Wr mice showed a vacuolated phenotype, which was significantly reverted by PROG treatment. In summary, PROG treatment during the early symptomatic stage of the disease caused a significant reduction of NADPHD-active motoneurons and astrocytes and also reduced vacuolated degenerating cells, suggesting that blockade of NO synthesis and oxidative damage may contribute to steroid neuroprotection.