ArticlePain2020
Spared nerve injury differentially alters parabrachial monosynaptic excitatory inputs to molecularly specific neurons in distinct subregions of the central amygdala.
Article in Pain, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- Cannabinoid modulation of central amygdala population dynamics during threat investigation.Nature communications · 2026Article
- Article
- Role of PBN-CeA Circuit in Paclitaxel-Induced Neuropathic Pain and Negative Emotions.CNS neuroscience & therapeutics · 2026Article
- Calcitonin Gene-Related Peptide (CGRP)-Containing Terminals in the Central Amygdala of Mice and Monkeys: Ultrastructural Analysis and Subsynaptic Expression of GluD1.The European journal of neuroscience · 2026Article
- Central amygdalar PKCδ neurons mediate fentanyl withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Neuropeptides in control of left-right neural circuits.Trends in neurosciences · 2026Review
- Recent progress in chronic pain-related negative emotions and cognitive dysfunction: insights into the mechanisms underlying neural circuitry.Frontiers in cellular neuroscience · 2026Review
- Article
- Neuro-immune regulation of sepsis-associated delirium via the PBN-CeA-spleen axis.Journal of neuroinflammation · 2025Article
- A nociceptive amygdala-striatal pathway modulating affective-motivational pain.Science advances · 2025Article
- Aversive experiences induce valence plasticity of instructive signals to change future learning rules in mice.Communications biology · 2025Article
- 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
- Delineation of the trigeminal-lateral parabrachial-central amygdala tract in humans.Imaging neuroscience (Cambridge, Mass.) · 2025Article
- Cells and circuits for amygdala neuroplasticity in the transition to chronic pain.Cell reports · 2024Article
- Dysfunction of Small-Conductance CaCells · 2024Article
- Ventromedial hypothalamic nucleus subset stimulates tissue thermogenesis via preoptic area outputs.Molecular metabolism · 2024Article
- The parabrachial to central amygdala pathway is critical to injury-induced pain sensitization in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Dynorphinergic Projections from the Central Amygdala to the Parabrachial Nucleus Regulate Itch.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Pain-related cortico-limbic plasticity and opioid signaling.Neuropharmacology · 2023Review
- Experience-dependent changes in affective valence of taste in male mice.Molecular brain · 2023Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dissecting the organization of circuit pathways involved in pain affect is pivotal for understanding behavior associated with noxious sensory inputs. The central nucleus of the amygdala (CeA) comprises distinct populations of inhibitory GABAergic neurons expressing a wide range of molecular markers. CeA circuits are associated with aversive learning and nociceptive responses. The CeA receives nociceptive signals directly from the parabrachial nucleus (PBn), contributing to the affective and emotional aspects of pain. Although the CeA has emerged as an important node in pain processing, key questions remain regarding the specific targeting of PBn inputs to different CeA subregions and cell types. We used a multifaceted approach involving transgenic reporter mice, viral vector-mediated optogenetics, and brain slice electrophysiology to delineate cell-type-specific functional organization of the PBn-CeA pathway. Whole-cell patch clamp recordings of molecularly defined CeA neurons while optogenetically driving long-range inputs originating from PBn revealed the direct monosynaptic excitatory inputs from PBn neurons to 3 major subdivisions of the CeA: laterocapsular (CeC), lateral (CeL), and medial (CeM). Direct monosynaptic excitatory inputs from PBn targeted both somatostatin-expressing (SOM+) and corticotropin-releasing hormone expressing (CRH+) neurons in the CeA. We find that monosynaptic PBn input is preferentially organized to molecularly specific neurons in distinct subdivisions of the CeA. The spared nerve injury model of neuropathic pain differentially altered PBn monosynaptic excitatory input to CeA neurons based on molecular identity and topographical location within the CeA. These results provide insight into the functional organization of affective pain pathways and how they are altered by chronic pain.
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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 Socratic graph.