<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-29T09:31:32Z</responseDate><request verb="GetRecord" identifier="oai:docta.ucm.es:20.500.14352/129134" metadataPrefix="oai_dc">https://docta.ucm.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:docta.ucm.es:20.500.14352/129134</identifier><datestamp>2025-12-17T00:56:15Z</datestamp><setSpec>com_20.500.14352_14</setSpec><setSpec>col_20.500.14352_15</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
   <dc:title>Bidirectional modulation of synaptic transmission by insulin-like growth factor-I</dc:title>
   <dc:creator>Noriega-Prieto, José A.</dc:creator>
   <dc:creator>Maglio,Laura E.</dc:creator>
   <dc:creator>Perez-Domper, Paloma</dc:creator>
   <dc:creator>Dávila, Juan Carlos</dc:creator>
   <dc:creator>Gutíerrez, Antonia</dc:creator>
   <dc:creator>Torres-Alemán, Ignancio</dc:creator>
   <dc:creator>Fernandez de Sevilla, David</dc:creator>
   <dc:subject>615</dc:subject>
   <dc:subject>Insulin-like growth factor-I</dc:subject>
   <dc:subject>LTD</dc:subject>
   <dc:subject>Spike-timing dependent plasticity</dc:subject>
   <dc:subject>Hebbian plasticity</dc:subject>
   <dc:subject>Hebbian plasticity</dc:subject>
   <dc:subject>Medicina</dc:subject>
   <dc:subject>3209.09 Psicofarmacología</dc:subject>
   <dc:description>Abstract
Insulin-like growth factor-I (IGF-I) plays a key role in the modulation of synaptic plasticity and is an essential factor in learning and memory processes. However, during aging, IGF-I levels are decreased, and the effect of this decrease in the induction of synaptic plasticity remains unknown. Here we show that the induction of N-methyl-D-aspartate receptor (NMDAR)-dependent long-term potentiation (LTP) at layer 2/3 pyramidal neurons (PNs) of the mouse barrel cortex is favored or prevented by IGF-I (10 nM) or IGF-I (7 nM), respectively, when IGF-I is applied 1 h before the induction of Hebbian LTP. Analyzing the cellular basis of this bidirectional control of synaptic plasticity, we observed that while 10 nM IGF-I generates LTP (LTPIGF-I) of the post-synaptic potentials (PSPs) by inducing long-term depression (LTD) of the inhibitory post-synaptic currents (IPSCs), 7 nM IGF-I generates LTD of the PSPs (LTDIGF-I) by inducing LTD of the excitatory post-synaptic currents (EPSCs). This bidirectional effect of IGF-I is supported by the observation of IGF-IR immunoreactivity at both excitatory and inhibitory synapses. Therefore, IGF-I controls the induction of Hebbian NMDAR-dependent plasticity depending on its concentration, revealing novel cellular mechanisms of IGF-I on synaptic plasticity and in the learning and memory machinery of the brain.</dc:description>
   <dc:description>Depto. de Fisiología</dc:description>
   <dc:description>Fac. de Medicina</dc:description>
   <dc:description>TRUE</dc:description>
   <dc:description>pub</dc:description>
   <dc:date>2025-12-16T12:30:36Z</dc:date>
   <dc:date>2025-12-16T12:30:36Z</dc:date>
   <dc:date>2024-06-07</dc:date>
   <dc:type>journal article</dc:type>
   <dc:type>VoR</dc:type>
   <dc:identifier>https://hdl.handle.net/20.500.14352/129134</dc:identifier>
   <dc:identifier>XXXX-XXXX</dc:identifier>
   <dc:identifier>10.3389/fncel.2024.1390663</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:relation>Noriega-Prieto, José Antonio, et al. «Bidirectional modulation of synaptic transmission by insulin-like growth factor-I». Frontiers in Cellular Neuroscience, vol. 18, junio de 2024, p. 1390663.  https://doi.org/10.3389/fncel.2024.1390663.</dc:relation>
   <dc:rights>Attribution 4.0 International</dc:rights>
   <dc:rights>http://creativecommons.org/licenses/by/4.0/</dc:rights>
   <dc:rights>open access</dc:rights>
   <dc:format>application/pdf</dc:format>
   <dc:publisher>Frontiers</dc:publisher>
</oai_dc:dc></metadata></record></GetRecord></OAI-PMH>