ROLE OF AMPA- NMDA-RECEPTORS AND BACK-PROPAGATING ACTION POTENTIALS IN SPIKE-TIMING DEPENDENT PLASTICITY. Export

@article{citeulike:6076179, abstract = {The cellular mechanisms that mediate spike-timing dependent plasticity (STDP) are largely unknown. We investigated in vitro in CA1 pyramidal neurons the contribution of AMPA and NMDA components of Schaffer collateral (SC) EPSPs (EPSPAMPA and EPSPNMDA) and of the back-propagating action potential (BAP) to the LTP induced by a STDP protocol that consisted in pairing an EPSP and a BAP. Transient blockade of EPSPAMPA with CNQX during the STDP protocol prevented LTP. Contrastingly LTP was induced under transient inhibition of EPSPAMPA by combining SC stimulation, an imposed EPSPAMPA-like depolarization and BAP, or by coupling the EPSPNMDA evoked under sustained depolarization ( approximately -40mV) and BAP. In Mg(2+)-free solution EPSPNMDA and BAP also produced LTP. Suppression of EPSPNMDA or BAP always prevented LTP. Thus, activation of NMDARs and BAP are required but not sufficient because AMPAR activation is also obligatory for STDP. However a transient depolarization of another origin that unblocks NMDARs and a BAP may also trigger LTP.}, author = {Fuenzalida, Marco and Fern\'{a}ndez de Sevilla, David and Couve, Alejandro and Buno, Washington}, citeulike-article-id = {6076179}, citeulike-linkout-0 = {http://dx.doi.org/10.1152/jn.00416.2009}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/19864442}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=19864442}, day = {28}, doi = {10.1152/jn.00416.2009}, issn = {1522-1598}, journal = {Journal of neurophysiology}, keywords = {hippocampus, ltp, molecular, nmda, stdp}, month = {October}, posted-at = {2009-11-05 19:13:33}, priority = {2}, title = {ROLE OF AMPA- NMDA-RECEPTORS AND BACK-PROPAGATING ACTION POTENTIALS IN SPIKE-TIMING DEPENDENT PLASTICITY.}, url = {http://dx.doi.org/10.1152/jn.00416.2009}, year = {2009} }

TY - JOUR ID - citeulike:6076179 L3 - citeulike-article-id:6076179 N2 - The cellular mechanisms that mediate spike-timing dependent plasticity (STDP) are largely unknown. We investigated in vitro in CA1 pyramidal neurons the contribution of AMPA and NMDA components of Schaffer collateral (SC) EPSPs (EPSPAMPA and EPSPNMDA) and of the back-propagating action potential (BAP) to the LTP induced by a STDP protocol that consisted in pairing an EPSP and a BAP. Transient blockade of EPSPAMPA with CNQX during the STDP protocol prevented LTP. Contrastingly LTP was induced under transient inhibition of EPSPAMPA by combining SC stimulation, an imposed EPSPAMPA-like depolarization and BAP, or by coupling the EPSPNMDA evoked under sustained depolarization ( approximately -40mV) and BAP. In Mg(2+)-free solution EPSPNMDA and BAP also produced LTP. Suppression of EPSPNMDA or BAP always prevented LTP. Thus, activation of NMDARs and BAP are required but not sufficient because AMPAR activation is also obligatory for STDP. However a transient depolarization of another origin that unblocks NMDARs and a BAP may also trigger LTP. JF - Journal of neurophysiology SN - 1522-1598 TI - ROLE OF AMPA- NMDA-RECEPTORS AND BACK-PROPAGATING ACTION POTENTIALS IN SPIKE-TIMING DEPENDENT PLASTICITY. KW - hippocampus KW - ltp KW - molecular KW - nmda KW - stdp AU - Fuenzalida, Marco AU - Fernández de Sevilla, David AU - Couve, Alejandro AU - Buno, Washington PY - 2009/10/28/ UR - http://dx.doi.org/10.1152/jn.00416.2009 ER -