ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Central amygdala metabotropic glutamate receptor 5 in the modulation of visceral pain.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
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The trial behind it
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Who cites it
56 citing papers in PubMed, 111 citations in OpenAlex.
- Trial
- Article
- Predicting Pain Using a Data-Driven Agent-Based Model of the Bilateral Central Amygdala.bioRxiv : the preprint server for biology · 2026Article
- Restoration of glutamate delta 1 signaling and excitatory inhibitory imbalance in the central amygdala in cisplatin induced neuropathic pain by cerebellin 1.Scientific reports · 2025Article
- Metabotropic Glutamate Receptor 5: A Potential Target for Neuropathic Pain Treatment.Current neuropharmacology · 2025Review
- This pain drives me crazy: Psychiatric symptoms in women with interstitial cystitis/bladder pain syndrome.World journal of psychiatry · 2024Article
- Optical EUS Activation to Relax Sensitized Micturition Response.Life (Basel, Switzerland) · 2023Article
- Hmgb1 Silencing in the Amygdala Inhibits Pain-Related Behaviors in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
- Inhibition of Canonical Transient Receptor Potential Channels 4/5 with Highly Selective and Potent Small-Molecule HC-070 Alleviates Mechanical Hypersensitivity in Rat Models of Visceral and Neuropathic Pain.International journal of molecular sciences · 2023Article
- The importance of the gut microbiome and its signals for a healthy nervous system and the multifaceted mechanisms of neuropsychiatric disorders.Frontiers in neuroscience · 2023Review
- Modulation of visceral pain by brain nuclei and brain circuits and the role of acupuncture: a narrative review.Frontiers in neuroscience · 2023Review
- Open source timed pressure control hardware and software for delivery of air mediated distensions in animal models.HardwareX · 2022Article
- Optogenetic Stimulation of the Anterior Cingulate Cortex Modulates the Pain Processing in Neuropathic Pain: A Review.Journal of molecular neuroscience : MN · 2022Review
- Sex Differences in CGRP Regulation and Function in the Amygdala in a Rat Model of Neuropathic Pain.Frontiers in molecular neuroscience · 2022Article
- The effect of amino acids on the bladder cycle: a concise review.Amino acids · 2022Review
- Article
- Agent-based modeling of the central amygdala and pain using cell-type specific physiological parameters.PLoS computational biology · 2021Article
- Transient receptor potential canonical 5 mediates inflammatory mechanical and spontaneous pain in mice.Science translational medicine · 2021Article
- Cellular, circuit and transcriptional framework for modulation of itch in the central amygdala.eLife · 2021Article
- Visceral pressure stimulator for exploring hollow organ pain: a pilot study.Biomedical engineering online · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Painful bladder syndrome is a debilitating condition that affects 3-6% of women in the United States. Multiple lines of evidence suggest that changes in CNS processing are key to the development of chronic bladder pain conditions but little is known regarding the underlying cellular, molecular, and neuronal mechanisms. Using a mouse model of distention-induced bladder pain, we found that the central nucleus of the amygdala (CeA) is a critical site of neuromodulation for processing of bladder nociception. Furthermore, we demonstrate that metabotropic glutamate receptor 5 (mGluR5) activation in the CeA induces bladder pain sensitization by increasing CeA output. Thus, pharmacological activation of mGluR5 in the CeA is sufficient to increase the response to bladder distention. Additionally, pharmacological blockade or virally mediated conditional deletion of mGluR5 in the CeA reduced responses to bladder distention suggesting that mGluR5 in the CeA is also necessary for these responses. Finally, we used optogenetic activation of the CeA and demonstrated that this caused a robust increase in the visceral pain response. The CeA-localized effects on responses to bladder distention are associated with changes in extracellular signal-regulated kinases 1/2 (ERK1/2) phosphorylation in the spinal cord. Overall, these data demonstrate that mGluR5 activation leads to increased CeA output that drives bladder pain sensitization.
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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.