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pubmed-article:11063994pubmed:abstractTextThe amplitude of backpropagating action potentials (BAPs) is attenuated, either activity- or neurotransmitter-dependently in the apical dendrite of hippocampal pyramidal neurons. To test the possibility that this BAP attenuation may contribute to regulating the inducibility of long-term potentiation (LTP), BAPs evoked by theta-burst stimulation (TBS), a standard protocol for LTP induction, to apical dendrite synapses were subjected to perturbation by conditioning stimuli to basal dendrite synapses. During this conditioned TBS (cTBS), the amplitude of BAPs was noticeably attenuated, but that of somatic action potentials was not. In the distal dendrite area, cTBS-induced LTP was much smaller than that induced by TBS. By contrast, no difference was observed between TBS- and cTBS-induced LTP in the proximal dendrite area. These findings suggest that the activity-dependent attenuation of BAPs, propagating along the apical dendrite, may serve to regulate hippocampal synaptic plasticity.lld:pubmed
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pubmed-article:11063994pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:11063994pubmed:articleTitlePossible regulatory role of dendritic spikes in induction of long-term potentiation at hippocampal schaffer collateral-CA1 synapses.lld:pubmed
pubmed-article:11063994pubmed:affiliationDepartment of Integrative Brain Science, Graduate School of Medicine, Kyoto University, 606-8501, Kyoto, Japan.lld:pubmed
pubmed-article:11063994pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:11063994pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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