mGlu1 receptor-induced LTD of NMDA receptor transmission selectively at schaffer collateral-CA1 synapses mediates metaplasticity

Mehdi Bhouri, Paul A. Farrow, Aneeta Motee, Xu Yan, Giuseppe Battaglia, Luisa Di Menna, Barbara Riozzi, Ferdinando Nicoletti, Stephen M. Fitzjohn, Zafar I. Bashir

Research output: Contribution to journalArticlepeer-review

Abstract

Hippocampal CA1 pyramidal neurons receive inputs from entorhinal cortex directly via the temporoammonic (TA) pathway and indirectly via the Schaffer collateral (SC) pathway from CA3. NMDARs at synapses of both pathways are critical for the induction of synaptic plasticity, information processing, and learning and memory. We now demonstrate that, in the rat hippocampus, activity-dependent mGlu1 receptor-mediated LTD (mGlu1-LTD) of NMDAR-mediated transmission (EPSCNMDA) at the SC-CA1 input prevents subsequent LTP of AMPAR-mediated transmission. In contrast, there was no activity-dependent mGlu1-LTD of EPSCNMDA at the TA-CA1 pathway, or effects on subsequent plasticity of AMPAR-mediated transmission. Therefore, the two major pathways delivering information to CA1 pyramidal neurons are subject to very different plasticity rules.

Original languageEnglish
Pages (from-to)12223-12229
Number of pages7
JournalJournal of Neuroscience
Volume34
Issue number36
DOIs
Publication statusPublished - Sep 3 2014

Keywords

  • LTD
  • Metaplasticity
  • NMDARs

ASJC Scopus subject areas

  • Neuroscience(all)

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