ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Mitochondrial reactive oxygen species are activated by mGluR5 through IP3 and activate ERK and PKA to increase excitability of amygdala neurons and pain behavior.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Interplay between genetics and lifestyle on pain susceptibility in women with fibromyalgia: the al-Ándalus project.Rheumatology (Oxford, England) · 2022Pooled it
- Mitochondrial dysfunction at the intersection of alcohol use disorder and chronic pain.Function (Oxford, England) · 2026Review
- Reverse electron transfer at mitochondrial complex I restrains dopaminergic neuron activity to promote early-life sleep inbioRxiv : the preprint server for biology · 2026Article
- The Double-Edged Effect of Connexins and Pannexins of Glial Cells in Central and Peripheral Nervous System After Nerve Injury.Molecular neurobiology · 2025Review
- A novel SIRT1 activator attenuates neuropathic pain by inhibiting spinal neuronal activation via the SIRT1-mGluR1/5 pathway.Cell biology and toxicology · 2025Article
- Oxidative Stress Promotes Liver Cancer Metastasis via RNF25-Mediated E-Cadherin Protein Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Endoplasmic reticular stress as an emerging therapeutic target for chronic pain: a narrative review.British journal of anaesthesia · 2024Review
- Amelioration of pain and anxiety in sleep-deprived rats by intra-amygdala injection of cinnamaldehyde.Sleep medicine: X · 2023Article
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- Activation of metabotropic glutamate receptor 1 regulates hippocampal CA1 region excitability in rats with status epilepticus by suppressing the HCN1 channel.Neural regeneration research · 2023Article
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- GPCR Intracellular Loop Regulation of Beta-Arrestin-Mediated Endosomal Signaling Dynamics.Journal of molecular neuroscience : MN · 2022Article
- Bioactive Compounds for Fibromyalgia-like Symptoms: A Narrative Review and Future Perspectives.International journal of environmental research and public health · 2022Review
- Bacopa monnieri attenuates glutamate-induced nociception and brain mitochondrial toxicity in Zebrafish.Metabolic brain disease · 2022Article
- Activity-regulated growth of motoneurons at the neuromuscular junction is mediated by NADPH oxidases.Frontiers in cellular neuroscience · 2022Article
- Hypoxia with inflammation and reperfusion alters membrane resistance by dynamically regulating voltage-gated potassium channels in hippocampal CA1 neurons.Molecular brain · 2021Article
- Blocking glutamate mGluBritish journal of pharmacology · 2021Article
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- Kappa opioid receptor activation in the amygdala disinhibits CRF neurons to generate pain-like behaviors.Neuropharmacology · 2021Article
- S-methyl-L-cysteine Protects against Antimycin A-induced Mitochondrial Dysfunction in Neural Cells via Mimicking Endogenous Methionine-centered Redox Cycle.Current medical science · 2020Article
15 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) such as superoxide are emerging as important signaling molecules in physiological plasticity but also in peripheral and spinal cord pain pathology. Underlying mechanisms and pain-related ROS signaling in the brain remain to be determined. Neuroplasticity in the amygdala plays a key role in emotional-affective pain responses and depends on group I metabotropic glutamate receptors (mGluRs) and protein kinases. Using patch-clamp, live-cell imaging, and behavioral assays, we tested the hypothesis that mitochondrial ROS links group I mGluRs to protein kinase activation to increase neuronal excitability and pain behavior. Agonists for mGluR1/5 (DHPG) or mGluR5 (CHPG) increased neuronal excitability of neurons in the laterocapsular division of the central nucleus of the amygdala (CeLC). DHPG effects were inhibited by an mGluR5 antagonist (MTEP), IP(3) receptor blocker (xestospongin C), or ROS scavengers (PBN, tempol), but not by an mGluR1 antagonist (LY367385) or NO synthase inhibitor (l-NAME). Tempol inhibited the effects of IP(3) but not those of a PKC activator, indicating that ROS activation was IP(3) mediated. Live-cell imaging in CeLC-containing brain slices directly showed DHPG-induced and synaptically evoked mitochondrial superoxide production. DHPG also increased pain-related vocalizations and spinal reflexes through a mechanism that required mGluR5, IP(3), and ROS. Combined application of inhibitors of ERK (U0126) and PKA (KT5720) was necessary to block completely the excitatory effects of a ROS donor (tBOOH). A PKC inhibitor (GF109203X) had no effect. Antagonists and inhibitors alone did not affect neuronal excitability. The results suggest an important role for the novel mGluR5- IP(3)-ROS-ERK/PKA signaling pathway in amygdala pain mechanisms.
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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.