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Titolo:
Generation and analysis of GluR5(Q636R) kainate receptor mutant mice
Autore:
Sailer, A; Swanson, GT; Perez-Otano, I; OLeary, L; Malkmus, SA; Dyck, RH; Dickinson-Anson, H; Schiffer, HH; Maron, C; Yaksh, TL; Gage, FH; OGorman, S; Heinemann, SF;
Indirizzi:
Salk Inst Biol Studies, Mol Neurobiol Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies La Jolla CA USA 92037 Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies, Gene Express Lab, La Jolla, CA 92037 USA Salk InstBiol Studies La Jolla CA USA 92037 Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies, Genet Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies La Jolla CA USA 92037 Lab, La Jolla, CA 92037 USA Univ Calif San Diego, Dept Pharmacol & Anesthesiol, La Jolla, CA 92093 USAUniv Calif San Diego La Jolla CA USA 92093 hesiol, La Jolla, CA 92093 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 20, volume: 19, anno: 1999,
pagine: 8757 - 8764
SICI:
0270-6474(19991015)19:20<8757:GAAOGK>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
TEMPORAL-LOBE EPILEPSY; SUBUNIT GLUR-B; SYNAPTIC ACTIVATION; HIPPOCAMPAL-NEURONS; CHANNEL PROPERTIES; CA2+ PERMEABILITY; BRAIN-DEVELOPMENT; MESSENGER-RNA; HIGH-AFFINITY; KAINIC ACID;
Keywords:
RNA editing; glutamate receptor; pain; dorsal root ganglia; gene targeting; Cre recombinase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Swanson, GT Salk Inst Biol Studies, Mol Neurobiol Lab, La Jolla, CA 92037 USA Salk Inst Biol Studies La Jolla CA USA 92037 la, CA 92037 USA
Citazione:
A. Sailer et al., "Generation and analysis of GluR5(Q636R) kainate receptor mutant mice", J NEUROSC, 19(20), 1999, pp. 8757-8764

Abstract

The physiological significance of RNA editing of transcripts that code forkainate-preferring glutamate receptor subunits is unknown, despite the fact that the functional consequences of this molecular modification have beenwell characterized in cloned receptor subunits. RNA editing of the codon that encodes the glutamine/arginine (Q/R) site in the second membrane domain(MD2) of glutamate receptor 5 (GluR5) and GluR6 kainate receptor subunits produces receptors with reduced calcium permeabilities and single-channel conductances. Approximately 50% of the GluR5 subunit transcripts from adult rat brain are edited at the Q/R site in MD2. To address the role of glutamate receptor mRNA editing in the brain, we have made two strains of mice with mutations at amino acid 636, the Q/R-editing site in GluR5, using embryonic stem cell-mediated transgenesis. GluR5(R-loxP/R-loxP) mice encode an arginine at the Q/R site of the GluR5 subunit, whereas GluR5(wt(loxP)/wt(loxP)) mice encode a glutamine at this site, similar to wild-type mice. Mutant animals do not exhibit developmental abnormalities, nor do they show deficits in the behavioral paradigms tested in this study. Kainate receptor current densities were reduced by a factor of six in acutely isolated sensory neurons of dorsal root ganglia from GluR5(R-loxP/R-loxP) mice compared with neurons from wild-type mice. However, the editing mutant mice did not exhibitaltered responses to thermal and chemical pain stimuli. Our investigationswith the GluR5-editing mutant mice have therefore defined a set of physiological processes in which editing of the GluR5 subunit is unlikely to play an important role.

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Documento generato il 01/04/20 alle ore 01:16:46