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Titolo:
Epilepsy, hyperalgesia, impaired memory, and loss of pre- and postsynapticGABA(B) responses in mice lacking GABA(B(1))
Autore:
Schuler, V; Luscher, C; Blanchet, C; Klix, N; Sansig, G; Klebs, K; Schmutz, M; Heid, J; Gentry, C; Urban, L; Fox, A; Spooren, W; Jaton, AL; Vigouret, JM; Pozza, M; Kelly, PH; Mosbacher, J; Froestl, W; Kaslin, E; Korn, R; Bischoff, S; Kaupmann, K; van der Putten, H; Bettler, B;
Indirizzi:
Novartis Pharma AG, TA Nervous Syst, CH-4002 Basel, Switzerland Novartis Pharma AG Basel Switzerland CH-4002 CH-4002 Basel, Switzerland Novartis Inst Med Sci, London WC1E 6B9, England Novartis Inst Med Sci London England WC1E 6B9 , London WC1E 6B9, England Univ Geneva, Dept Pharmacol APSIC, CH-1211 Geneva, Switzerland Univ Geneva Geneva Switzerland CH-1211 PSIC, CH-1211 Geneva, Switzerland Univ Geneva, Dept Physiol, CH-1211 Geneva 4, Switzerland Univ Geneva Geneva Switzerland 4 Physiol, CH-1211 Geneva 4, Switzerland Univ Geneva, Dept Neurol, CH-1211 Geneva 4, Switzerland Univ Geneva Geneva Switzerland 4 t Neurol, CH-1211 Geneva 4, Switzerland
Titolo Testata:
NEURON
fascicolo: 1, volume: 31, anno: 2001,
pagine: 47 - 58
SICI:
0896-6273(20010719)31:1<47:EHIMAL>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR ANTAGONISTS; PRESYNAPTIC INHIBITION; RAT HIPPOCAMPUS; HETEROMERIC COMPLEXES; IN-VITRO; ADENOSINE; RELEASE; HETERODIMERIZATION; RETENTION; SUBTYPES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Bettler, B Novartis Pharma AG, TA Nervous Syst, CH-4002 Basel, SwitzerlandNovartis Pharma AG Basel Switzerland CH-4002 sel, Switzerland
Citazione:
V. Schuler et al., "Epilepsy, hyperalgesia, impaired memory, and loss of pre- and postsynapticGABA(B) responses in mice lacking GABA(B(1))", NEURON, 31(1), 2001, pp. 47-58

Abstract

GABA(B) (gamma -aminobutyric acid type B) receptors are important for keeping neuronal excitability under control. Cloned GABA(B) receptors do not show the expected pharmacological diversity of native receptors and it is unknown whether they contribute to pre- as well as postsynaptic functions. Here, we demonstrate that Balb/c mice lacking the GABA(B(1)) subunit are viable, exhibit spontaneous seizures, hyperalgesia, hyperlocomotor activity, andmemory impairment. Upon GABA(B) agonist application, null mutant mice showneither the typical muscle relaxation, hypothermia, or delta EEG waves. These behavioral findings are paralleled by a loss of all biochemical and electrophysiological GABA(B) responses in null mutant mice. This demonstrates that GABA(B(1)) is an essential component of pre- and postsynaptic GABA(B) receptors and casts doubt on the existence of proposed receptor subtypes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/01/20 alle ore 09:56:58