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Titolo:
Epileptogenesis and enhanced prepulse inhibition in GABA(B1)-deficient mice
Autore:
Prosser, HM; Gill, CH; Hirst, WD; Grau, E; Robbins, M; Calver, A; Soffin, EM; Farmer, CE; Lanneau, C; Gray, J; Schenck, E; Warmerdam, BS; Clapham, C; Reavill, C; Rogers, DC; Stean, T; Upton, N; Humphreys, K; Randall, A; Geppert, M; Davies, CH; Pangalos, MN;
Indirizzi:
GlaxoSmithKline Pharmaceut, Neurol Ctr Excellence Drug Discovery, Harlow CM19 5AW, Essex, England GlaxoSmithKline Pharmaceut Harlow Essex England CM19 5AW , Essex, England GlaxoSmithKline Pharmaceut, Psychiat Ctr Excellence Drug Discovery, HarlowCM19 5AW, Essex, England GlaxoSmithKline Pharmaceut Harlow Essex England CM19 5AW , Essex, England GlaxoSmithKline Pharmaceut, Genet Res, Harlow CM19 5AW, Essex, England GlaxoSmithKline Pharmaceut Harlow Essex England CM19 5AW , Essex, England GlaxoSmithKline Pharmaceut, Safety Assessment, Harlow CM19 5AW, Essex, England GlaxoSmithKline Pharmaceut Harlow Essex England CM19 5AW , Essex, England GlaxoSmithKline Pharmaceut, Lab Anim Sci, Harlow CM19 5AW, Essex, England GlaxoSmithKline Pharmaceut Harlow Essex England CM19 5AW , Essex, England
Titolo Testata:
MOLECULAR AND CELLULAR NEUROSCIENCE
fascicolo: 6, volume: 17, anno: 2001,
pagine: 1059 - 1070
SICI:
1044-7431(200106)17:6<1059:EAEPII>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
FUNCTIONAL GABA(B) RECEPTOR; HIPPOCAMPAL SLICE; RAT; EXPRESSION; SCHIZOPHRENIA; SUBUNIT; HETERODIMERIZATION; IDENTIFICATION; BACLOFEN; CURRENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Pangalos, MN GlaxoSmithKline Pharmaceut, Neurol Ctr Excellence Drug Discovery, New Frontiers Sci Pk,3rd Ave, Harlow CM19 5AW, Essex, England GlaxoSmithKline Pharmaceut New Frontiers Sci Pk,3rd Ave Harlow Essex England CM19 5AW
Citazione:
H.M. Prosser et al., "Epileptogenesis and enhanced prepulse inhibition in GABA(B1)-deficient mice", MOL CELL NE, 17(6), 2001, pp. 1059-1070

Abstract

The recent cloning of two GABA(B) receptor subunits, GABA(B1) and GABA(B2), has raised the possibility that differences in GABA(B) receptor subunit composition may give rise to pharmacologically or functionally distinct receptors. If present, such molecular diversity could permit the selective targeting of GABA(B) receptor subtypes specifically involved in pathologies such as drug addiction, spasticity, pain, and epilepsy. To address these issues we have developed a GABA(B1) subunit knockout mouse using gene targeting techniques. In the brains of GABA(B1) null mice, all pre- and postsynaptic GABA(B) receptor function was absent demonstrating that the GABA(B1) subunit is essential for all GABA(B) receptor-mediated mechanisms. Despite this, GABA(B1) null mice appeared normal at birth, although by postnatal week four their growth was retarded and they developed a generalized epilepsy that resulted in premature death. In addition, GABA(B1) heterozygote animals showed enhanced prepulse inhibition responses compared to littermate controls,suggesting that GABA(B1) deficient mice exhibit increased sensorimotor gating mechanisms. These data suggest that GABA(B) receptor antagonists may beof benefit in the treatment of psychiatric and neurological disorders in which attentional processing is impaired.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/20 alle ore 06:21:29