Pain Mechanisms and Treatments

The paper models spinal dorsal horn processing of tactile stimuli to explain why certain stimuli cause allodynia and how spinal cord stimulation can alleviate it.

This study shows that mice lacking both Substance P and CGRP signaling still exhibit normal pain responses, indicating these peptides are not essential for pain transmission.

This study shows that TLR4+ dermal fibroblasts induce acute and transitional pain states in mice through inflammatory and calcium signaling mechanisms.

This study identifies Brs3-expressing neurons in the parabrachial nucleus as a key population involved in heat hypersensitivity during persistent pain.

This study shows that mast cell-derived chymases are crucial for resolving inflammatory pain by degrading CCL9 and promoting myeloid cell recruitment in mice.

The paper investigates how tonic pain modulates phasic pain-predictive cues using a virtual-reality paradigm and EEG, finding that tonic pain reconfigures internal representations of pain associations.

This study identifies CD34/PDGFRA+ cells in human dorsal root ganglia as putative telocytes, characterizes their subclusters, and shows their proximity to neurons and blood vessels without ultrastructural variation.

The paper examines how spinal nociceptive output changes in acute and neuropathic pain states using calcium imaging.

The paper investigates how neural variability relates to pain discriminability across EEG datasets and finds it is a reliable and selective indicator.

The paper investigates the effects of inflammatory soup on sensory neuron excitability using human and mouse models, finding minimal changes and suggesting that in vitro modeling of peripheral sensitization is complex.

This paper shows that diroximel fumarate (DRF) reduces MGO-induced pain hypersensitivity in mice by activating Nrf2 and decreasing ISR activation in DRG neurons.

This study establishes a heat-induced pain model in Fabry disease and identifies a heat shock protein-TRPA1 regulatory axis as a key mechanism.

The paper investigates how astrocytes modulate primary afferent axon excitability through Ca2+-binding proteins, leading to ectopic firing in a muscle pain model.

This study uses cuff algometry to compare pain and paresthesia responses to varying pressure and duration parameters in pain-free individuals, finding distinct patterns for each symptom.

The paper tests the hypothesis that phasic and tonic pain serve distinct functions in adaptive behavior using a virtual reality foraging task with EEG measurements.

This paper investigates how schwannoma-induced pain is mediated by mechanosensitive ion channels and shows that GsMTx-4 can reduce mechanosensitivity in a schwannomatosis model.

This study evaluates the analgesic potential of AS1 in mice, finding it selectively abolishes second phase formalin nocifensive behavior without affecting other pain models.

This study shows that blocking spinal α2 adrenoceptors in rats can promote anti-nociception, challenging the traditional view that α2 activation is anti-nociceptive.

This study develops a therapeutic protein, UbiquiNaV, that reduces NaV1.8 channel expression in sensory neurons, alleviating pain in preclinical models.

The paper demonstrates that efferent signaling along nociceptive terminals increases during inflammation, leading to enhanced calcium signaling and mediator release in remote terminals.

This study identifies QTL and candidate genes for ethanol-induced analgesia in BXD mouse strains using behavioral and bioinformatic analyses.

This study identifies two thalamic nuclei mediating different aspects of cold pain responses in mice through viral genetics and physiology.

This study assesses the test-retest reliability and intra-individual consistency of pain modulation measures and links CPM response variability to effective connectivity in the descending pain modulation system.

This study shows repetitive neonatal pain increases spinal cord DNA methylation of the μ-opioid receptor gene Mor-1 in rats.

This study identifies a brain circuit involving the dorsal lateral septum and lateral hypothalamic area that drives stress-induced analgesia through opioid-dependent modulation of pain pathways.

The paper identifies persistent interferon signaling via the MNK1/2-eIF4E pathway as a driver of sensory neuron plasticity and pain in arthritis.

This paper identifies mechanisms of excitatory-inhibitory balance dysregulation in spinal cord dorsal horn subcircuits that contribute to allodynia, revealing subcircuit-specific vulnerabilities and potential therapeutic targets.

This study identifies IL-10's role in upregulating delta opioid receptor to prevent pain relapse during remission.