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Titolo:
Gadolinium reduces AMPA receptor desensitization and deactivation in hippocampal neurons
Autore:
Lei, S; MacDonald, JF;
Indirizzi:
Univ Toronto, Dept Physiol, Toronto, ON M5S 1A8, Canada Univ Toronto Toronto ON Canada M5S 1A8 ysiol, Toronto, ON M5S 1A8, Canada Univ Toronto, Dept Pharmacol, Toronto, ON M5S 1A8, Canada Univ Toronto Toronto ON Canada M5S 1A8 macol, Toronto, ON M5S 1A8, Canada
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 1, volume: 86, anno: 2001,
pagine: 173 - 182
SICI:
0022-3077(200107)86:1<173:GRARDA>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTAMATE-RECEPTOR; KAINATE RECEPTORS; KINETIC-PROPERTIES; NMDA RESPONSES; CHANNELS; CYCLOTHIAZIDE; MODULATION; MAGNESIUM; PATCHES; GLYCINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: MacDonald, JF Univ Toronto, Dept Physiol, Med Sci Bldg, Toronto, ON M5S 1A8, Canada Univ Toronto Med Sci Bldg Toronto ON Canada M5S 1A8 , Canada
Citazione:
S. Lei e J.F. MacDonald, "Gadolinium reduces AMPA receptor desensitization and deactivation in hippocampal neurons", J NEUROPHYS, 86(1), 2001, pp. 173-182

Abstract

The actions of the trivalent cation Gd3+ on whole cell AMPA receptor-mediated currents were studied in isolated hippocampal neurons, in nucleated or outside-out patches taken from cultured hippocampal neurons, and on miniature excitatory postsynaptic currents (mEPSCs) recorded in cultured hippocampal neurons. Glutamate, AMPA, or kainate was employed to activate AMPA receptors. Applications of relatively low concentrations of Gd3+ (0.1-10 muM) substantially enhanced steady-state whole cell glutamate and kainate-evoked currents without altering peak currents, suggesting that desensitization wasreduced. However, higher concentrations (>30 muM) depressed steady-state currents, indicating an underlying inhibition of channel activity. Lower concentrations of Gd3+ also increased the potency of peak glutamate-evoked currents without altering that of steady-state currents. An ultrafast perfusion system and nucleated patches were then used to better resolve peak glutamate-evoked currents. Low concentrations of Gd3+ reduced peak currents, enhanced steady-state currents, and slowed the onset of desensitization, providing further evidence that this cation reduces desensitization. In the presence of cyclothiazide, a compound that blocks desensitization, a low concentration Gd3+ inhibited both peak and steady-state currents, indicating that Gd3+ both reduces desensitization and inhibits these currents. Gd3+ reducedthe probability of channel opening at the peak of the currents but did notalter the single channel conductance calculated using nonstationary variance analysis. Recovery from desensitization was enhanced, and glutamate-evoked current activation and deactivation were slowed by Gd3+. The Gd3+ induced reduction in desensitization did not require the presence of the GluR2 subunit as this effect was seen in hippocampal neurons from GluR2 null-mutantmice. Gd3+ reduced the time course of decay of mEPSCs perhaps as a consequence of its slowing of AMPA receptor deactivation although an increase in the frequency of mEPSCs also suggested enhanced presynaptic release of transmitter. These results demonstrate that Gd3+ potently reduces AMPA receptor desensitization and mimics a number of the properties of the positive modulators of AMPA receptor desensitization such as cyclothiazide.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 16:38:22