{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:21:50Z","timestamp":1791296510618,"version":"4.1.0"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,1,12]],"date-time":"2007-01-12T00:00:00Z","timestamp":1168560000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,1,15]]},"abstract":"<jats:p>During wakefulness and sleep, neurons in the neocortex emit action potentials tonically or in rhythmic bursts, respectively. However, the role of synchronized discharge patterns is largely unknown. We have recently shown that pairings of excitatory postsynaptic potentials (EPSPs) and action potential bursts or single spikes lead to long\u2010term depression (burst\u2010LTD) or long\u2010term potentiation, respectively. In this study, we elucidate the cellular mechanisms of burst\u2010LTD and characterize its functional properties. Whole\u2010cell patch\u2010clamp recordings were obtained from layer V pyramidal cells in somatosensory cortex of juvenile rats <jats:italic>in vitro<\/jats:italic> and composite EPSPs and EPSCs were evoked extracellularly in layers II\/III. Repetitive burst\u2010pairings led to a long\u2010lasting depression of EPSPs and EPSCs that was blocked by inhibitors of metabotropic glutamate group 1 receptors, phospholipase C, protein kinase C (PKC) and calcium release from the endoplasmic reticulum, and that required an intact machinery for endocytosis. Thus, burst\u2010LTD is induced via a Ca<jats:sup>2+<\/jats:sup>\u2010 and phosphatidylinositol\u2010dependent activation of PKC and expressed through phosphorylation\u2010triggered endocytosis of AMPA receptors. Functionally, burst\u2010LTD is inversely related to EPSP size and bursts dominate single spikes in determining the sign of synaptic plasticity. Thus burst\u2010firing constitutes a signal by which coincident synaptic inputs are proportionally downsized. Overall, our data thus suggest a mechanism by which synaptic weights can be reconfigured during non\u2010rapid eye movement sleep.<\/jats:p>","DOI":"10.1113\/jphysiol.2006.123588","type":"journal-article","created":{"date-parts":[[2006,11,3]],"date-time":"2006-11-03T01:34:21Z","timestamp":1162517661000},"page":"471-479","source":"Crossref","is-referenced-by-count":74,"title":["Cellular mechanisms of burst firing\u2010mediated long\u2010term depression in rat neocortical pyramidal 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