ArticlePNAS nexus2024
Loss of synaptopodin impairs mGluR5 and protein synthesis-dependent mGluR-LTD at CA3-CA1 synapses.
Article in PNAS nexus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- GRASPing experience-dependent protein expression signatures enriched for hippocampal engram cell synapses.Science advances · 2026Article
- The ISR downstream effector ATF4 promotes mGluR-dependent long-term depression and associated behavior.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The perforant pathway and CA3-Schaffer collateral afferents coordinate to regulate spatial learning.Communications biology · 2026Article
- Metabotropic Glutamate Receptor-Dependent Synaptic Plasticity in Age-Related Neurodegenerative Disorders.Neural plasticity · 2026Review
- Incubation with tau aggregates increases hippocampal circuit excitability and enhances long-term depression in acute mouse hippocampal slices.Frontiers in neural circuits · 2025Article
- Synaptopodin is required for long-term depression at Schaffer collateral-CA1 synapses.Molecular brain · 2024Article
- Synaptopodin: a key regulator of Hebbian plasticity.Frontiers in cellular neuroscience · 2024Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Metabotropic glutamate receptor-dependent long-term depression (mGluR-LTD) is an important form of synaptic plasticity that occurs in many regions of the central nervous system and is the underlying mechanism for several learning paradigms. In the hippocampus, mGluR-LTD is manifested by the weakening of synaptic transmission and elimination of dendritic spines. Interestingly, not all spines respond or undergo plasticity equally in response to mGluR-LTD. A subset of dendritic spines containing synaptopodin (SP), an actin-associated protein is critical for mGluR-LTD and protects spines from elimination through mGluR1 activity. The precise cellular function of SP is still enigmatic and it is still unclear how SP contributes to the functional aspect of mGluR-LTD despite its modulation of the structural plasticity. In this study, we show that the lack of SP impairs mGluR-LTD by negatively affecting the mGluR5-dependent activity. Such impairment of mGluR5 activity is accompanied by a significant decrease of surface mGluR5 level in SP knockout (SPKO) mice. Intriguingly, the remaining mGluR-LTD becomes a protein synthesis-independent process in the SPKO and is mediated instead by endocannabinoid signaling. These data indicate that the postsynaptic protein SP can regulate the locus of expression of mGluR-LTD and provide insight into our understanding of spine/synapse-specific plasticity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.