Pain Mechanisms and Treatments

The paper shows that the input-output relation of primary nociceptive neurons depends on the morphology of their peripheral terminals and how multiple terminals integrate noxious stimuli.

This study shows that aging reduces morphine's pain-relieving effect and lowers μ-opioid receptor levels in the rat midbrain PAG, affecting both males and females.

This study investigates the role of NK1R spinal neurons in itch using a Tacr1CreER mouse line, showing their involvement in modulating itch behavior through coexpression with GRPR.

This study inhibits the colon epithelium and primary afferent neurons in a mouse model of IBD to assess their role in pain hypersensitivity, finding both reduce visceral sensitivity.

The paper identifies sex differences in nociceptor translatomes, revealing sex-specific prostaglandin signaling differences in male and female mice.

This study shows that SARS-CoV-2 Spike protein blocks VEGF-A/NRP-1 signaling, reducing pain and potentially contributing to asymptomatic transmission.

The paper characterizes transgenic mouse lines for selectively targeting glial cells in dorsal root ganglia and identifies two suitable lines for studying satellite glial cells and macrophages.

This study identifies sex-specific neuroendocrine mechanisms in chronic pain, showing that prolactin receptor signaling in sensory neurons contributes to hyperalgesic priming in females but not males.

This paper introduces PAWS, a machine-vision tool for automated pain measurement in mice, showing it can distinguish painful from non-painful stimuli and quantify pain severity.

The paper investigates the role of NK1R activation in maintaining latent sensitization, finding that NK1R antagonists prevent opioid-induced allodynia in chronic pain models.

This study shows reducing MCT1 worsens diabetic peripheral neuropathy in mice, suggesting caution in using MCT1 inhibitors for diabetic patients.

The paper compares neuronal subpopulations in mouse and human dorsal root ganglia using RNAscope in situ hybridization, finding differences in CGRP and P2X3R expression and other markers.

The paper characterizes immune responses in a neuropathic pain mouse model and develops a web-based tool for transcriptional data-mining of peripheral neuroimmune interactions.

The paper tests if Src family kinases maintain latent sensitization in rats with inflammatory or neuropathic pain and finds that inhibiting SFKs prevents opioid antagonist-induced allodynia.

This study shows that preventing CRMP2 SUMOylation reduces mechanical allodynia in female neuropathic pain models but not in males or other pain types.

This study examines epigenetic changes in the mouse prefrontal cortex over time following nerve injury, identifying persistent DNA methylation alterations associated with acute to chronic pain transition.

This study identifies a specific subset of sensory neurons expressing PAR2 that mediate mechanical and affective pain behaviors, clarifying the cellular basis of PAR2-evoked pain.

The paper investigates whether resting alpha frequency is a reliable biomarker for predicting sensitivity to prolonged pain in healthy individuals.

This study shows that TNF-α activated fibroblast-like synoviocytes sensitize knee neurons in vitro, contributing to inflammatory pain in arthritis.

This study identifies neuronal LXR regulation of neuregulin-1 and its role in neuron-Schwann cell communication in obesity-associated neuropathy.

The paper identifies distinct neural pathways from the lateral parabrachial nucleus that mediate different aspects of the pain response, including escape behaviors and aversive memory.

This study investigates how bone cancer affects the peripheral encoding of mechanical pressure stimuli by comparing sensory afferent responses in healthy and cancer-induced bone pain rats.

This study shows type I interferons act directly on nociceptors via MNK-eIF4E signaling to cause pain hypersensitivity in mice, linking viral infections to pain and neuropathies.

The paper identifies a CeA-LPB pathway that regulates pain perception and shows its suppression in chronic pain.

The paper compares transcriptomes of native and cultured human and mouse dorsal root ganglia, finding reduced neuronal gene expression in culture but presence of key pharmacological targets.

This study identifies PI16 as a non-neuronal factor produced by fibroblasts that promotes neuropathic pain by modulating endothelial barrier function and leukocyte infiltration.

The paper identifies brain networks mediating stimulus-pain relationships using high-dimensional mediation analysis in fMRI data from 284 humans.

This study assesses evoked and spontaneous pain following tooth pulp injury in mice using behavioral and molecular techniques to uncover pain mechanisms.

The paper shows that voluntary physical activity prevents chronic pain susceptibility in mice fed a high-fat diet and sedentary, through changes in nucleus accumbens gene expression.

This study identifies a consistent neural signature of acute pain in healthy volunteers through a large-scale fMRI meta-analysis, highlighting a core set of brain regions involved in pain processing.