Pain Mechanisms and Treatments

The paper identifies SLC45A4 as a pain-related gene encoding a neuronal polyamine transporter through GWAS and functional studies.

The paper investigates social interactions in mice in naturalistic conditions, finding that mice in pain are socially avoided, challenging previous findings of empathy in rodent models.

This study investigates the role of LGI1 in pain regulation using mouse models, finding that LGI1 ablation in spinal neurons exacerbates neuropathic pain behaviors, suggesting a spinal mechanism for its role in pain sensitivity.

This study investigates the role of CeAGA neurons in acute and late-phase neuropathic pain, finding they have distinct effects on pain thresholds and anxiety behaviors.

The paper reanalyzes pain prediction using sociodemographic, psychological, and fMRI data, finding that combining multiple measures can predict interindividual pain intensity differences.

This study demonstrates the use of engineered zinc finger repressors delivered via AAV to reduce SCN9A expression in preclinical models, showing efficacy in reducing neuropathic pain.

This study shows that satellite glial cells modulate proprioceptor activity via Gq GPCR signaling and purinergic receptors, suggesting therapeutic targets for sensorimotor disorders.

The paper investigates how spinal cord organization influences the perception of the Thermal Grill Illusion, finding that spatial arrangement of warm and cold stimuli affects burning sensations.

The paper identifies Nageotte nodules in diabetic painful neuropathy DRGs, showing they contain dead neurons and are linked to pain and sensory loss.

This study shows that oxytocin's analgesic mechanism is altered in Parkinson's disease model rats, leading to hyperalgesia due to reduced oxytocin signaling in the PVN.

This study investigates the effect of blocking Aβ fibers on pain perception and nociceptive withdrawal reflexes in humans, finding that Aβ fibers may contribute to pain and reflex signaling.

This study shows that peripheral nerve injury preferentially eliminates specific DRG neuron subpopulations, particularly non-peptidergic nociceptors, and links this loss to neurotrophic support.

The paper identifies persistent changes in nociceptor mRNA translation following hyperalgesic priming and shows Gpr88 and Metrn regulate this state.

The paper identifies analgesic targets in mouse sensory neurons by analyzing translatomes in somata and terminals under different pain conditions.

This study investigates how genomic and transcriptomic profiles interact with brain morphology to influence individual differences in pain sensitivity using multi-omics data from 432 participants.

The paper identifies distinct transcriptional responses in microglia during opioid exposure and neuropathic pain, highlighting injury-specific mechanisms and the absence of opioid-induced transcriptional changes.

The paper investigates how endocrine signaling and neuroimmune communication regulate neonatal pain, finding that GH signaling via STAT1 influences inflammatory pain through a novel neuroimmune loop.

The paper uses light-sensitive drugs to show that mGlu5 receptor blockade in specific brain regions has different effects on pain, with some areas reducing analgesia and others enhancing it.

This study identifies NGF-TrkA-PI3K signaling in keratinocyte-nociceptor interactions as a driver of obesity-induced small fiber neuropathy and suggests targeting these interactions as a therapeutic strategy.

This study identifies a brainstem circuit involving LPBN and RVM neurons that mediates pain-induced suppression of itch in mice.

This study shows that a cAMP signaling pathway can induce long-term hyperexcitability in nociceptors, which may contribute to persistent pain.

This study evaluates three potential treatments for cancer-induced bone pain in mice, finding that dual inhibition of NGF and TNF significantly reduces pain-related behaviors.

The paper isolates nerve terminals from NaV1.9 knockout mice and performs proteomic analysis to identify dysregulated pathways in neuropathic pain signaling.

This paper shows that inhibiting specific spinal cord Hsp90 isoforms enhances opioid pain relief while reducing tolerance and side effects.

This study shows ephrin-B2 promotes nociceptive plasticity and hyperalgesic priming in mice and humans through MNK-eIF4E signaling in DRG neurons.

This study shows that BDNF contributes to activity-induced muscle pain in male mice but not female mice, with no sex differences in BDNF expression changes.

This study shows that ZFHX3 deficiency in mice leads to altered pain responses and reduced cautious-like behavior in both sexes, with female mice showing specific hypoalgesia to mechanical stimuli and hyperalgesia to heat.

This study shows that CBD3063, a CRMP2 modulator, reduces OA pain in rodents by decreasing CaV2.2 membrane expression and neural activity.