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This Article Free via Open Access: OA OA Full Text Full Text (PDF) Supplemental Data OA All Versions of this Article: 586/3/779    most recent jphysiol.2007.147017v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Campanac, E. Articles by Debanne, D. PubMed PubMed Citation Articles by Campanac, E. Articles by Debanne, D. Related Collections Neuroscience

¹ INSERM U641
² Université de la Méditerranée, Faculté de médecine secteur nord, IFR 11, Marseille, F-13916, France

Long-term plasticity of dendritic integration is induced in parallel with long-term potentiation (LTP) or depression (LTD) based on presynaptic activity patterns. It is, however, not clear whether synaptic plasticity induced by temporal pairing of pre- and postsynaptic activity is also associated with synergistic modification in dendritic integration. We show here that the spike timing-dependent plasticity (STDP) rule accounts for long-term changes in dendritic integration in CA1 pyramidal neurons in vitro. Positively correlated pre- and postsynaptic activity (delay: +5/+50 ms) induced LTP and facilitated dendritic integration. Negatively correlated activity (delay: –5/–50 ms) induced LTD and depressed dendritic integration. These changes were not observed following positive or negative pairing with long delays (> ±50 ms) or when NMDA receptors were blocked. The amplitude–slope relation of the EPSP was facilitated after LTP and depressed after LTD. These effects could be mimicked by voltage-gated channel blockers, suggesting that the induced changes in EPSP waveform involve the regulation of voltage-gated channel activity. Importantly, amplitude–slope changes induced by STDP were found to be input specific, indicating that the underlying changes in excitability are restricted to a limited portion of the dendrites. We conclude that STDP is a common learning rule for long-term plasticity of both synaptic transmission and dendritic integration, thus constituting a form of functional redundancy that insures significant changes in the neuronal output when synaptic plasticity is induced.

(Received 19 October 2007; accepted after revision 26 November 2007; first published online 29 November 2007)
Corresponding author D. Debanne: Université de la Méditerranée, Faculté de médecine secteur nord, IFR 11, Marseille, F-13916, France. Email: dominique.debanne{at}univmed.fr

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