Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Dysfunctions in mice by NMDA receptor point mutations NR1(N598Q) and NR1(N598R)
Autore:
Single, FN; Rozov, A; Burnashev, N; Zimmermann, F; Hanley, DF; Forrest, D; Curran, T; Jensen, V; Hvalby, O; Sprengel, R; Seeburg, PH;
Indirizzi:
Max Planck Inst Med Res, Dept Mol Neurosci, D-69120 Heidelberg, Germany Max Planck Inst Med Res Heidelberg Germany D-69120 0 Heidelberg, Germany Max Planck Inst Med Res, Dept Cell Physiol, D-69120 Heidelberg, Germany Max Planck Inst Med Res Heidelberg Germany D-69120 0 Heidelberg, Germany Univ Heidelberg, Ctr Mol Biol, D-69120 Heidelberg, Germany Univ Heidelberg Heidelberg Germany D-69120 , D-69120 Heidelberg, Germany Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA Johns Hopkins Univ Baltimore MD USA 21287 Neurol, Baltimore, MD 21287 USA Mt Sinai Sch Med, Dept Human Genet, New York, NY 10029 USA Mt Sinai Sch Med New York NY USA 10029 uman Genet, New York, NY 10029 USA St Jude Childrens Res Hosp, Dept Dev Neurobiol, Memphis, TN 38105 USA St Jude Childrens Res Hosp Memphis TN USA 38105 ol, Memphis, TN 38105 USA Univ Oslo, Inst Basic Med Sci, Dept Neurophysiol, N-0317 Oslo, Norway UnivOslo Oslo Norway N-0317 Sci, Dept Neurophysiol, N-0317 Oslo, Norway
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 7, volume: 20, anno: 2000,
pagine: 2558 - 2566
SICI:
0270-6474(20000401)20:7<2558:DIMBNR>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
DEPENDENT SYNAPTIC PLASTICITY; CEREBELLAR GRANULE CELLS; D-ASPARTATE RECEPTORS; SOMATOSENSORY CORTEX; NR2 SUBUNITS; MUTANT MICE; GLUR-B; CHANNEL; GENE; DEFICIENT;
Keywords:
NMDA receptor; gene targeting; Cre-loxP; Mg2+ block; Ca2+ influx; coincidence detection; respiration; nurturing; barrel cortex; LTP;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Sprengel, R Max Planck Inst Med Res, Dept Mol Neurosci, Jahnstr 29, D-69120 Heidelberg, Germany Max Planck Inst Med Res Jahnstr 29 Heidelberg Germany D-69120
Citazione:
F.N. Single et al., "Dysfunctions in mice by NMDA receptor point mutations NR1(N598Q) and NR1(N598R)", J NEUROSC, 20(7), 2000, pp. 2558-2566

Abstract

NMDA receptors in mice were mutated by gene targeting to substitute asparagine (N) in position 598 of the NR1 subunit to glutamine (Q) or arginine (R). Animals expressing exclusively the mutated NR1 alleles, NR1(Q/Q) and NR1(-/R) mice, developed a perinatally lethal phenotype mainly characterized by respiratory failure. The dysfunctions were partially rescued in heterozygous mice by the presence of pure wild-type receptors. Thus, NR1(+/Q) mice exhibited reduced life expectancy, with females being impaired in nurturing;NR1(+/R) mice displayed signs of underdevelopment such as growth retardation and impaired righting reflex, and died before weaning. We analyzed the key properties of NMDA receptors, high Ca2+ permeability, and voltage-dependent Mg2+ block, in the mutant mice. Comparison of the complex physiologicaland phenotypical changes observed in the different mutants indicates that properties controlled by NR1 subunit residue N598 are important for autonomic brain functions at birth and during postnatal development. We conclude that disturbed NMDA receptor signaling mediates a variety of neurological phenotypes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 17:03:43