ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Activation conditions for the induction of metabotropic glutamate receptor-dependent long-term depression in hippocampal CA1 pyramidal cells.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 13 citations in OpenAlex.
- Synaptic plasticity rules with physiological calcium levels.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Hippocampal mGluR1-dependent long-term potentiation requires NAADP-mediated acidic store CaScience signaling · 2018Article
- Functional organization of postsynaptic glutamate receptors.Molecular and cellular neurosciences · 2018Review
- Long term potentiation, but not depression, in interlamellar hippocampus CA1.Scientific reports · 2018Article
- Layer-specific potentiation of network GABAergic inhibition in the CA1 area of the hippocampus.Scientific reports · 2016Article
- Gating of NMDA receptor-mediated hippocampal spike timing-dependent potentiation by mGluR5.Neuropharmacology · 2012Article
- Multiple functions of endocannabinoid signaling in the brain.Annual review of neuroscience · 2012Review
- Mechanisms of induction and maintenance of spike-timing dependent plasticity in biophysical synapse models.Frontiers in computational neuroscience · 2010Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Two forms of homosynaptic long-term depression (LTD) are distinguished in hippocampal CA1 pyramidal cells, one which is NMDA receptor dependent and the other metabotropic glutamate receptor (mGluR) dependent. Although the molecular processes involved in mGluR-LTD are well characterized, the conditions of circuit activation required for its induction remain unclear. We show that mGluR-LTD cannot be induced in synaptically coupled CA3-CA1 pyramidal cell pairs. Experiments to address the underlying mechanisms indicate that, even when glutamate transporters are blocked, one presynaptic cell releases insufficient glutamate to evoke an mGluR-mediated current in a connected CA1 cell. These findings imply that extrasynaptic diffusion is not a limiting factor and are consistent with a sparse distribution of functional mGluRs in the dendritic tree of pyramidal cells. Thus, the discharge of multiple Schaffer collaterals to a targeted cell is necessary for mGluR-LTD. Our experiments indicate that approximately eight CA3 inputs to a CA1 pyramidal cell must be activated to induce mGluR-LTD.
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