Pain Mechanisms and Treatments

The paper identifies a diencephalic circuit involving the lateral habenula and lateral preoptic area that mediates opioid analgesia without reinforcement.

This study uses single-cell RNA sequencing to analyze spinal cord microglia responses to nerve injury, identifying sex- and time-specific changes and a role for ApoE in neuropathic pain.

The paper identifies unified neural pathways that gate affective pain and multisensory innate threat signals to the amygdala, revealing their role in aversive perception.

The paper examines individual differences in pain perception and finds no brain activation differences linked to reported pain intensity, despite BOLD signal sensitivity to stimulus intensity within individuals.

The paper identifies a stable core of neurons and dynamic ensembles in the anterior cingulate cortex that represent pain, showing impaired pattern separation after nerve injury.

This study shows that non-SUMOylated CRMP2 forms an endocytic complex to internalize NaV1.7 channels, and inhibiting this complex restores sodium currents in mice with neuropathic pain.

This paper maps sympathetic adrenergic and sensory peptidergic axons in mouse limb bones to identify region-specific innervation patterns related to bone pain, repair, and homeostasis.

The paper uses optogenetics to assess how non-peptidergic C-fiber afferents contribute to aversive behaviors before and after nerve injury.

This study shows that over-expressing a soluble colony-stimulating factor 1 receptor reduces neuropathic pain by decreasing microgliosis and macrophage accumulation in mice.

The paper identifies individual cortical signatures of pain in chronic pain patients using fMRI and linear mixed effects models, revealing unique patterns of pain encoding in specific brain regions.

The paper was withdrawn due to retraction of conclusions by the authors.

The paper identifies Arc as an activity-dependent gene involved in neurogenic inflammation through intercellular signaling via extracellular vesicles.

This study identifies microvascular neogenesis in somatosensory cortex of chronic pain models, suggesting altered vascular architecture with potential implications for CP diagnosis and treatment.

This study shows that peripheral CaV2.2 channels in skin are essential for thermal hyperalgesia but not mechanical hypersensitivity after capsaicin exposure in mice.

This study develops AI-bRNN to decode spontaneous pain from calcium signals in mice, assessing pain intensity and analgesic efficacy while distinguishing pain from itch.

The paper shows that increasing spinal acetylcholine levels through low-dose AChE inhibitors reduces mechanical allodynia in neuropathic mice.

The paper identifies a new population of CGRP-expressing interneurons in the spinal cord dorsal horn that contribute to mechanical hypersensitivity after nerve injury.

This study identifies opioid-dependent inhibition of neurotransmitter release as the primary mechanism of analgesia in NaV1.7 null mutants in mice and humans.

The paper identifies a subpopulation of glycinergic interneurons in the spinal cord regulated by Shank2, whose dysfunction contributes to pain hypersensitivity in ASD mouse models.

The paper investigates movement-induced analgesia through five experiments on 130 healthy humans, showing it results from multiple neural mechanisms rather than a single one.

This study shows that reduced dopaminergic inhibition in the anterior cingulate cortex contributes to neuropathic pain by increasing neuronal excitability.

The paper tests the Neural Pain Signature (NPS) in breathlessness and somatomotor tasks, finding overlap but not equivalence, and identifies limitations in its specificity.

The paper identifies silent cold-sensing neurons that become active in neuropathic pain and contribute to cold allodynia through peripheral sensitization.

The paper creates interactome maps of ligand-receptor interactions between peripheral cell types and sensory neurons in mouse and human disease states, identifying potential therapeutic targets like EGFR.

This paper shows anthrax toxin can target and modulate pain by acting on nociceptive neurons through ANTXR2, with potential for new pain therapeutics.

The paper uses TRAP to analyze translatomes of excitatory and inhibitory neurons in mouse spinal cords, finding neuropeptide genes associated with modality-specific processing and showing little translatome change in neuropathic pain.

The paper identifies kenpaullone as a compound that enhances KCC2 expression and reduces pathologic pain by restoring inhibitory neurotransmission in mouse models.

This study shows that ER stress in DRG neurons contributes to pain in MS and that ER stress modulators can reduce pain hypersensitivity in an EAE model.

This study identifies 6-9 Hz cortical oscillations as a reliable biomarker for detecting chronic pain in rats by comparing individual pre-injury baselines to post-injury power changes.

This study identifies claudin-12's role in maintaining myelin and blood-nerve barriers, showing its deficiency causes mechanical hypersensitivity and painful neuropathy in male mice.