ArticleAutophagy2025
Trans-synaptic signaling through GRID1/glutamate receptor delta-1 and CBLN1/cerebellin-1 facilitates autophagic flux in central amygdala and prevents chronic pain.
Article in Autophagy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- GluN2D NMDA Receptors: Bridging Physiology and Pathology.Biological psychiatry · 2026Review
- Review
- Molecular basis for ligand-gating of the human GluD1 receptor.bioRxiv : the preprint server for biology · 2026Article
- GluD1 at the synaptic crossroads: from domain structure to circuit dysfunction.Acta pharmacologica Sinica · 2026Review
- Glutamate Delta 1 Receptor in Synapses, Circuits, and Disease.The European journal of neuroscience · 2026Review
- Transsynaptic complex dysfunction in the hippocampus of Alzheimer's disease patients.Frontiers in aging neuroscience · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Central amygdala (CeA) is a component of the spino-parabrachio-amygdala nociceptive pathway. Neuroplasticity in this pathway, such as increased cellular excitability and excitatory neurotransmission, play a key role in the development and persistence of chronic pain. However, the underlying mechanisms of neuroplastic changes in the CeA remain poorly understood. We recently demonstrated that GRID1/GluD1 (glutamate ionotropic receptor delta type subunit 1) and its binding partner CBLN1 (cerebellin 1 precursor) are downregulated in models of inflammatory and neuropathic pain. Furthermore, we have shown that GRID1-CBLN1 signaling regulates autophagy in multiple brain regions. Here, we tested the causal relationship between GRID1-CBLN1 downregulation, macroautophagy impairment, and subsequent hyperalgesia, using models of inflammatory and neuropathic pain. During pain, the downregulation of GRID1 and CBLN1 was accompanied by neuroplastic changes, as evidenced by an increase in excitatory neurotransmission and AMPA receptor (AMPAR) expression. In addition, significant downregulation of BECN1 and upregulation of SQSTM1 and MAP1LC3B, demonstrating impaired autophagic flux, were observed in the pain state. These changes appear to be cell type-specific, as observed by the higher localization of BECN1 and LAMP1, a marker for autolysosomes, to PRKCD
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What Socratic holds
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 Socratic graph.