Reply to Meredith and Groen: Role of AMPA and NMDA Receptors and Back-Propagating Action Potentials in Spike Timing–Dependent Plasticity

Abstract

Letters to the EditorReply to Meredith and Groen: Role of AMPA and NMDA Receptors and Back-Propagating Action Potentials in Spike Timing–Dependent PlasticityMarco Fuenzalida, David Fernández de Sevilla, Alejandro Couve, and Washington BuñoMarco FuenzalidaCentro de Neurobiología y Plasticidad del Desarrollo, Facultad de Ciencias, Universidad Valparaiso, Valparaiso, Chile, David Fernández de SevillaDepartamento de Anatomía, Histología y Neurociencia, Facultad de Medicina, Universidad Autónoma de Madrid, Madrid, Spain; and , Alejandro CouveCentro de Neurobiología y Plasticidad del Desarrollo, Facultad de Ciencias, Universidad Valparaiso, Valparaiso, Chile, and Washington BuñoInstituto Cajal, Consejo Superior de Investigaciones Científicas; Published Online:01 Apr 2010https://doi.org/10.1152/jn.00170.2010MoreSectionsPDF (28 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations reply: In their letter Meredith and Groen (2010) emphasize the role of GABAergic inhibition in controlling dendritic excitability and depolarization in pyramidal neurons and, consequently, in regulating the induction threshold of long-term potentiation (LTP). In particular they stress the requirement of a burst of postsynaptic back-propagating action potentials in the induction of spike timing–dependent plasticity (STDP) when inhibition is functional in vitro. We totally agree with their view. Indeed countless reports show that LTP is more readily induced when dendritic excitability and depolarization are not regulated by inhibition.In our experiments GABAergic inhibition was blocked to analyze the role of glutamatergic excitatory postsynaptic potentials (EPSPs) and back-propagating action potentials in the genesis of LTP by STDP (Fuenzalida et al. 2007, 2010). In these reports a single action potential was sufficient to induce LTP with STDP protocols.We point out that recently Kwag and Paulsen (2009) reported that an STDP-like protocol—which simulates the theta rhythm and generates a single back-propagating action potential per theta cycle added to an EPSP—was able to induce LTP not only with intact inhibition but also without inhibition in CA1 pyramidal cells in vitro.Therefore the degree of postsynaptic depolarization needed for back-propagation of action potentials and dendritic Ca2+ spike generation required for STDP may be attained in special conditions without the need of postsynaptic action potential bursts.REFERENCES Fuenzalida M , Fernández de Sevilla D , Buño W. Changes of the EPSP waveform regulate the temporal window for spike-timing-dependent plasticity. J Neurosci 27: 11940–11948, 2007.Crossref | PubMed | ISI | Google Scholar Fuenzalida M , Fernández de Sevilla D , Couve A , Buño W. Role of AMPA and NMDA receptors and back-propagating action potentials in spike timing–dependent plasticity. J Neurophysiol 103: 47–54, 2010.Link | ISI | Google Scholar Kwag J , Paulsen O. The timing of external input controls the sign of plasticity at local synapses. Nat Neurosci 12: 1219–1221, 2009.Crossref | PubMed | ISI | Google Scholar Meredith RM , Groen MR. Inhibition of action potential backpropagation during postnatal development of the hippocampus. J Neurophysiol 103: 2313, 2010.Link | ISI | Google ScholarAUTHOR NOTESAddress for reprint requests and other correspondence: W. Buño, Instituto Cajal, Consejo Superior de Investigaciones Científicas, Avenida Doctor Arce 37, 28002 Madrid, Spain (E-mail: [email protected]csic.es). Download PDF Previous Back to Top FiguresReferencesRelatedInformation More from this issue > Volume 103Issue 4April 2010Pages 2314-2314 Copyright & PermissionsCopyright © 2010 the American Physiological Societyhttps://doi.org/10.1152/jn.00170.2010History Published online 1 April 2010 Published in print 1 April 2010 Metrics