ArticleFrontiers in pharmacology2022
Kappa Opioid Receptor Blockade in the Amygdala Mitigates Pain Like-Behaviors by Inhibiting Corticotropin Releasing Factor Neurons in a Rat Model of Functional Pain.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Persistent effects of repeated adolescent and adult heroin vapor inhalation in female Wistar rats.Psychopharmacology · 2026Article
- Kappa opioid receptor antagonism in neuropsychiatry: from molecular mechanisms to clinical prospects.European archives of psychiatry and clinical neuroscience · 2026Review
- Kappa opioid receptors in excitatory spinal neurons gate acute pain: evidence from mouse and human.bioRxiv : the preprint server for biology · 2026Article
- Neuropeptides in control of left-right neural circuits.Trends in neurosciences · 2026Review
- The Dynorphin/-Opioid Receptor System at the Interface of Hyperalgesia/Hyperkatifeia and Addiction.Current addiction reports · 2025Review
- Early-life pain alters excitability of corticotropin-releasing factor-expressing neurons in the central amygdala and stress-induced hypersensitivity during adolescence.Frontiers in behavioral neuroscience · 2025Article
- Emerging Psychotropic Drug for the Treatment of Trigeminal Pain: Salvinorin A.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Limitations and potential of κOR biased agonists for pain and itch management.Neuropharmacology · 2024Review
- Cells and circuits for amygdala neuroplasticity in the transition to chronic pain.Cell reports · 2024Article
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- Dysfunction of Small-Conductance CaCells · 2024Article
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- A "double-edged" role for type-5 metabotropic glutamate receptors in pain disclosed by light-sensitive drugs.bioRxiv : the preprint server for biology · 2024Article
- Impaired amygdala astrocytic signaling worsens neuropathic pain-associated neuronal functions and behaviors.Frontiers in pharmacology · 2024Article
- Hmgb1 Silencing in the Amygdala Inhibits Pain-Related Behaviors in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- Studies on diketopiperazine and dipeptide analogs as opioid receptor ligands.European journal of medicinal chemistry · 2023Article
- Dynorphin/kappa opioid receptor system regulation on amygdaloid circuitry: Implications for neuropsychiatric disorders.Frontiers in systems neuroscience · 2022Review
- Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Functional pain syndromes (FPS) occur in the absence of identifiable tissue injury or noxious events and include conditions such as migraine, fibromyalgia, and others. Stressors are very common triggers of pain attacks in various FPS conditions. It has been recently demonstrated that kappa opioid receptors (KOR) in the central nucleus of amygdala (CeA) contribute to FPS conditions, but underlying mechanisms remain unclear. The CeA is rich in KOR and encompasses major output pathways involving extra-amygdalar projections of corticotropin releasing factor (CRF) expressing neurons. Here we tested the hypothesis that KOR blockade in the CeA in a rat model of FPS reduces pain-like and nocifensive behaviors by restoring inhibition of CeA-CRF neurons. Intra-CeA administration of a KOR antagonist (nor-BNI) decreased mechanical hypersensitivity and affective and anxiety-like behaviors in a stress-induced FPS model. In systems electrophysiology experiments in anesthetized rats, intra-CeA application of nor-BNI reduced spontaneous firing and responsiveness of CeA neurons to peripheral stimulation. In brain slice whole-cell patch-clamp recordings, nor-BNI increased feedforward inhibitory transmission evoked by optogenetic and electrical stimulation of parabrachial afferents, but had no effect on monosynaptic excitatory transmission. Nor-BNI decreased frequency, but not amplitude, of spontaneous inhibitory synaptic currents, suggesting a presynaptic action. Blocking KOR receptors in stress-induced FPS conditions may therefore represent a novel therapeutic strategy.
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