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Titolo:
Glutamine synthetase activity and expression are not affected by the development of motor neuronopathy in the G93A SOD-1/ALS mouse
Autore:
Fray, AE; Dempster, S; Williams, RE; Cookson, MR; Shaw, PJ;
Indirizzi:
Univ Newcastle Upon Tyne, Dept Neurol, Newcastle Upon Tyne NE1 7RU, Tyne &Wear, England Univ Newcastle Upon Tyne Newcastle Upon Tyne Tyne & Wear England NE1 7RU
Titolo Testata:
MOLECULAR BRAIN RESEARCH
fascicolo: 1-2, volume: 94, anno: 2001,
pagine: 131 - 136
SICI:
0169-328X(20011019)94:1-2<131:GSAAEA>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYOTROPHIC-LATERAL-SCLEROSIS; SPINAL-CORD; OXIDATIVE STRESS; BRAIN; PROTEINS; MICE; MUTATIONS; DISEASE; DAMAGE; SOD1;
Keywords:
glutamine synthetase; transgenic mouse; motor neurone disease; amyotrophic lateral sclerosis; motor neuronopathy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Fray, AE Lilly Res Ctr Ltd, Erl Wood Manor, Windlesham GU20 6PH, Surrey, England Lilly Res Ctr Ltd Erl Wood Manor Windlesham Surrey England GU20 6PH
Citazione:
A.E. Fray et al., "Glutamine synthetase activity and expression are not affected by the development of motor neuronopathy in the G93A SOD-1/ALS mouse", MOL BRAIN R, 94(1-2), 2001, pp. 131-136

Abstract

The expression and activity of the enzyme glutamine synthetase (GS) were examined in the G93A/SOD-1 transgenic mouse model of progressive motor neuronopathy to investigate the mechanisms underlying degeneration of the motor neurones. Clinical signs appeared in G93A/SOD-1 mice at around 90 days, with severe spasticity and loss of self-righting reflex from 120 to 150 days of age. GS expression was examined using western blotting in primary astrocyte cultures derived from newborn (P1-2) G93A/SOD-1 mice and their non-transgenic littermates and in lower spinal cord from animals at 30, 60 and 90 days of age and disease end-stage (120-150 days). There were no differences in the levels of GS expression in the transgenic mice compared to the unaffected littermates at any of the disease stages examined. GS activity was measured spectrophotometric ally in spinal cord extracts at these disease stages. There was a decrease in V-max at 60 days compared to 30 days in both groups of mice (3.48 +/- 0.58 cf. 6.43 +/- 1.83 mmol/h/mg protein; non-transgenic littermates), with GS activity highest at end-stage (9.38 +/- 0.71 mmol/h/mg protein cf. 7.64 +/- 0.42 mmol/h/mg protein in littermates). Conversely, K-m was transiently increased at 60 days (2.53 +/- 0.26 mM cf. 1.32 +/- 0.20 in littermates), remaining within the range of 30 day measurements from 90 days onwards. There were no differences in V-max or K-m values between the G93A/SOD-1 mice and their unaffected non-transgenic littermates at any of the disease stages examined. We conclude that there is no evidence that a change in glutamine synthetase activity or expression contributes to the progressive neurodegeneration observed in the G93A/SOD-1 mice. (C) 2001 Elsevier Science BY All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 13:29:18