ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2024
The parabrachial to central amygdala pathway is critical to injury-induced pain sensitization in mice.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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34 citing papers in PubMed, 62 citations in OpenAlex.
- Article
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- The basolateral amygdala decodes visceral pain and itch via distinct circuits and molecules.Nature communications · 2026Article
- A Dnmt3a-Mediated Epigenetic Mechanism for Chronic-Pain-Induced Behaviors of Negative Emotion in Mice.Cells · 2026Article
- Parabrachial bombesin receptor subtype 3 neurons facilitate heat hypersensitivity in persistent pain.bioRxiv : the preprint server for biology · 2026Article
- Early life stress induces brain-wide electrical network predisposition to migraine.The journal of headache and pain · 2026Article
- Optogenetic LTP Manipulation and Mathematical Modeling to Investigate Value Plasticity of the Instructive Signal in Mice.Bio-protocol · 2026Article
- Central amygdalar PKCδ neurons mediate fentanyl withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Predicting Pain Using a Data-Driven Agent-Based Model of the Bilateral Central Amygdala.bioRxiv : the preprint server for biology · 2026Article
- Molecular Signatures of Maladaptive Plasticity in the Amygdala in a Rat Model of Chronic Neuropathic Pain.Cells · 2026Article
- Parabrachial CGRP Neurons Regulate Opioid Reinforcement.bioRxiv : the preprint server for biology · 2026Article
- Electroacupuncture alleviates depression and gastrointestinal dysfunction by rebalancing GABAergic activity in the central amygdala.World journal of psychiatry · 2026Article
- Chronic stress increases the susceptibility to chronic vulvar pain following acute vulvar inflammation in a preclinical model of vulvodynia.Molecular brain · 2026Article
- Recent progress in chronic pain-related negative emotions and cognitive dysfunction: insights into the mechanisms underlying neural circuitry.Frontiers in cellular neuroscience · 2026Review
- Contribution of proprioceptors in the mesencephalic trigeminal nucleus and their surrounding astrocytes to acidic saline-induced chronic jaw muscle pain in rodents.Frontiers in cellular neuroscience · 2026Article
- Obesity-driven low-grade chronic inflammation as a mechanistic bridge to chronic pain: from adipose tissue remodeling to central sensitization.Frontiers in immunology · 2026Review
- Pain Perception and Modulation: Fundamental Neurobiology and Recent Advances.The European journal of neuroscience · 2025Review
- Calcitonin Gene-Related Peptide (CGRP)-Expressing Neurons in the External Lateral Parabrachial Area Regulate Pain-Induced Sleep Disturbances.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Aversive experiences induce valence plasticity of instructive signals to change future learning rules in mice.Communications biology · 2025Article
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12 authors at 2 institutions in 1 country.
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Abstract
The spino-ponto-amygdaloid pathway is a major ascending circuit relaying nociceptive information from the spinal cord to the brain. Potentiation of excitatory synaptic transmission in the parabrachial nucleus (PBN) to central amygdala (CeA) pathway has been reported in rodent models of persistent pain. However, the functional significance of this pathway in the modulation of the somatosensory component of pain was recently challenged by studies showing that spinal nociceptive neurons do not target CeA-projecting PBN cells and that manipulations of this pathway have no effect on reflexive-defensive somatosensory responses to peripheral noxious stimulation. Here, we showed that activation of CeA-projecting PBN neurons is critical to increase both stimulus-evoked and spontaneous nociceptive responses following an injury in male and female mice. Using optogenetic-assisted circuit mapping, we confirmed a functional excitatory projection from PBN→CeA that is independent of the genetic or firing identity of CeA cells. We then showed that peripheral noxious stimulation increased the expression of the neuronal activity marker Fos in CeA-projecting PBN neurons and that chemogenetic inactivation of these cells decreased behavioral hypersensitivity in models of neuropathic and inflammatory pain without affecting baseline nociception. Lastly, we showed that chemogenetic activation of CeA-projecting PBN neurons is sufficient to induced bilateral hypersensitivity without injury. Together, our results indicate that the PBN→CeA pathway is a key modulator of pain-related behaviors that can increase reflexive-defensive and affective-motivational responses to somatosensory stimulation in injured states without affecting nociception under normal physiological conditions.
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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 Socratic graph.