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Titolo:
Bidirectional synaptic plasticity correlated with the magnitude of dendritic calcium transients above a threshold
Autore:
Cormier, RJ; Greenwood, AC; Connor, JA;
Indirizzi:
Univ New Mexico, Sch Med, Dept Neurosci, Albuquerque, NM 87131 USA Univ New Mexico Albuquerque NM USA 87131 rosci, Albuquerque, NM 87131 USA
Titolo Testata:
JOURNAL OF NEUROPHYSIOLOGY
fascicolo: 1, volume: 85, anno: 2001,
pagine: 399 - 406
SICI:
0022-3077(200101)85:1<399:BSPCWT>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; METABOTROPIC GLUTAMATE RECEPTORS; HIPPOCAMPAL-NEURONS; PYRAMIDAL CELLS; POSTSYNAPTIC CALCIUM; PERFORANT PATH; VISUAL-CORTEX; CA1 NEURONS; INDUCTION; STIMULATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Cormier, RJ Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 St Louis, MO 63110 USA
Citazione:
R.J. Cormier et al., "Bidirectional synaptic plasticity correlated with the magnitude of dendritic calcium transients above a threshold", J NEUROPHYS, 85(1), 2001, pp. 399-406

Abstract

The magnitude of postsynaptic Ca2+ transients is thought to affect activity-dependent synaptic plasticity associated with learning and memory. Large Ca2+ transients have been implicated in the induction of long-term potentiation (LTP), while smaller Ca2+ transients have been associated with long-term depression (LTD). However, a direct relationship has not been demonstrated between Ca2+ measurements and direction of synaptic plasticity in the same cells, using one induction protocol. Here, we used glutamate iontophoresis to induce Ca2+ transients in hippocampal CA1 neurons injected with the Ca2+- indicator fura-2. Test stimulation of one or two synaptic pathways before and after iontophoresis showed that the direction of synaptic plasticity correlated with glutamate-induced Ca2+ levels above a threshold, below which no plasticity occurred (similar to 180 nM). Relatively low Ca2+ levels (180-500 nM) typically led to LTD of synaptic transmission and higher levels (>500 nM) often led to LTP. Failure to show plasticity correlated with Ca2+ levels in two distinct ranges: <180 nM and <similar to>450-600 nM, whileonly LTD occurred between these ranges. Our data support a class of modelsin which failure of Ca2+ transients to affect transmission may arise either from insufficient Ca2+ to affect Ca2+-sensitive proteins regulating synaptic strength through opposing activities or from higher Ca2+ levels that reset activities of such proteins without affecting the net balance of activities. Our estimates of the threshold Ca2+ level for LTD (similar to 180 nM)and for the transition from LTD to LTP (similar to 540 nM) may assist in constraining the molecular details of such models.

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Documento generato il 09/04/20 alle ore 00:19:36