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Titolo:
CA2-KINASE-C POTENTIATION OF RECOMBINANT NMDA RECEPTORS( INFLUX AMPLIFIES PROTEIN)
Autore:
ZHENG X; ZHANG L; WANG AP; BENNETT MVL; ZUKIN RS;
Indirizzi:
YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT NEUROSCI,1300 MORRIS PK AVE BRONX NY 10461 YESHIVA UNIV ALBERT EINSTEIN COLL MED,DEPT NEUROSCI BRONX NY 10461
Titolo Testata:
The Journal of neuroscience
fascicolo: 22, volume: 17, anno: 1997,
pagine: 8676 - 8686
SICI:
0270-6474(1997)17:22<8676:CPORNR>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHYL-D-ASPARTATE; LONG-TERM POTENTIATION; XENOPUS OOCYTES; HIPPOCAMPAL-NEURONS; SPLICE VARIANTS; NR1 SUBUNIT; CALCIUM PERMEABILITY; GLUTAMATE RECEPTORS; MOLECULAR DIVERSITY; MESSENGER-RNA;
Keywords:
PROTEIN KINASE C; NMDA RECEPTORS; ALTERNATIVE RNA SPLICING; TPA; BAPTA; XENOPUS OOCYTE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
55
Recensione:
Indirizzi per estratti:
Citazione:
X. Zheng et al., "CA2-KINASE-C POTENTIATION OF RECOMBINANT NMDA RECEPTORS( INFLUX AMPLIFIES PROTEIN)", The Journal of neuroscience, 17(22), 1997, pp. 8676-8686

Abstract

Protein kinase C (PKC) potentiates NMDA receptors in hippocampal, trigeminal, and spinal neurons. Although PKC phosphorylates the NMDA receptor subunit NR1 at four residues within the C terminal splice cassette C1, the molecular mechanisms underlying PKC potentiation of NMDA responses are not yet known. The present study examined the role of Ca2+ in PKC potentiation of recombinant NMDA receptors expressed in Xenopusoocytes. We found that Ca2+ influx through PKC-potentiated NMDA receptors can further increase the NMDA response (''Ca2+ amplification''). Ca2+ amplification required a rise in intracellular Ca2+ concentrationat or near the intracellular end of the channel and was independent of Ca2+-activated Cl- current. Ca2+ amplification depended on extracellular Ca2+ concentration during NMDA application and not during PKC activation. Ca2+ amplification was reduced by the membrane-permeant Ca2+-chelating agent BAPTA-AM. Mutant receptors with greatly reduced Ca2+ permeability did not exhibit Ca2+ amplification. Receptors containing the NR1 N-terminal splice cassette showed more Ca2+ amplification, possibly because of their larger basal current and therefore greater Ca2+ influx. Contrary to expectation, splicing out the two C-terminal splice cassettes of NR1 enhanced PKC potentiation in a manner independent of extracellular Ca2+. This observation indicates that PKC potentiationdoes not require phosphorylation of the C1 cassette of the NR1 subunit. PKC potentiation of NMDA receptors in vivo is likely to be affectedby Ca2+ amplification of the potentiated signal; the degree of amplification will depend in part on alternative splicing of the NR1 subunit, which is regulated developmentally and in a cell-specific manner.

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Documento generato il 07/07/20 alle ore 18:33:28