Pain Mechanisms and Treatments

The paper identifies Ptf1a neurons in the spinal cord that inhibit cutaneous afferents, and their loss leads to chronic itch and increased skin sensitivity.

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.

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.

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The paper was withdrawn due to retraction of conclusions by the authors.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

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

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

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

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 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.

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.