Pain Mechanisms and Treatments

The paper uses SCD patient-derived iPSCs to study sensory neuron function and identifies plasma factors that sensitize neurons to pain stimuli.

This study shows Schwann cells promote sensory neuron excitability during development by secreting prostaglandin E2, which is essential for normal sodium channel expression and action potential firing.

The paper identifies Mrgprd-expressing DRG neurons as a driver of pain hypersensitivity in a mouse model of PDN and shows targeting these neurons can reverse mechanical allodynia.

This study investigates cellular and synaptic changes in the central nucleus of the amygdala (CeA) in a mouse model of chronic muscle pain and identifies CeA-SST neurons as key players in central sensitization.

This study shows spinal microglia amplify neuronal activity in inflammatory pain via the P2Y12 receptor, suggesting a therapeutic target for pain management.

This study identifies the cellular distribution of matrisome genes in murine and human dorsal root ganglia, revealing their potential role in neuronal signaling and pain.

This study identifies an inhibitory neural circuit from CeA-PKCδ neurons to the zona incerta that bidirectionally modulates pain-related behaviors in mice.

This study shows that male mice benefit from intrathecal BMSCs and TGF-β1 for CIPN relief, while female mice do not, highlighting sex differences in pain modulation.

This study identifies the kynurenine metabolic pathway as a key factor in sustaining neuropathic pain through interactions between meningeal dendritic cells and astrocytes.

The paper uses scRNA-seq to identify subtype-specific transcriptomic changes in DRG neurons of Pirt-EGFPf mice under neuropathic pain conditions.

This study identifies reactive astrocytes controlled by Wnt5a signaling as critical for opioid-induced hyperalgesia development in mice.

This study identifies mTOR and NPY/Y2R signaling as key drivers of neuropathic pain by enhancing nociceptor excitability through transcriptional induction of NPY.

This study shows that early life pain exposure in rats increases functional connectivity in the somatosensory and medial prefrontal cortex, correlating with heightened pain hypersensitivity in adulthood.

The paper investigates how the deletion of the Tac1 gene affects kinase phosphorylation in spinal cord tissue, revealing altered signaling pathways linked to pain modulation and inflammatory responses.

This study shows that parvalbumin protein (PVp) buffers calcium to maintain tonic firing in PV neurons, and its reduction after nerve injury leads to mechanical allodynia.

The paper identifies cis-regulatory elements in dorsal root ganglion neurons that show differential chromatin accessibility and TF binding after nerve injury, linking them to chronic pain.

The paper identifies spinal VGLUT3 neurons as drivers of visceral mechanical allodynia but not visceromotor reflexes in mice with GI inflammation.

The paper identifies a parabrachial-to-amygdala circuit mediated by CGRP that drives hemispheric lateralization of visceral pain processing in mice.

This study shows reducing Adenylyl Cyclase 1 activity decreases morphine-induced hyperalgesia and inflammatory pain in mice without affecting morphine's analgesic effects.

This study shows that neuronal C-reactive protein activates FcγRI signaling in DRG neurons, contributing to neuropathic pain, and that disrupting this pathway reduces pain in a rat model.

The paper investigates the role of mu-opioid receptor-expressing neurons in the periaqueductal gray in modulating pain and itch behaviors through optogenetic and chemogenetic manipulations.

This study investigates the role of Tacr1-expressing ON cells in the RVM in modulating pruriceptive transmission, finding they inhibit itch despite being pronociceptive.

The paper identifies a novel subtype of reactive astrocytes, HIPAs, critical for HIV-associated pain pathogenesis in mice and humans.

The paper integrates metabolomic, proteomic, and phospho-proteomic analyses of dorsal root ganglia from DPN donors and controls to identify molecular changes associated with diabetic neuropathic pain.

This study shows that adolescent ethanol exposure in mice leads to long-term pain sensitivity, neuroinflammation, and serotonergic deficits, with microglial activation in the dorsal raphe nucleus as a key driver.

This study compares immune responses to inflammation in neonatal and adult rats, finding differences in immune cell recruitment and cytokine profiles that may explain reduced nociceptive hypersensitivity in neonates.

This study investigates how prenatal hypoxia-ischemia injury affects spinal nociceptive circuitry in rabbits, finding increased nociceptive afferents and enhanced mechanical and thermal sensitivity.

The paper profiles transcriptomic and proteomic data from NaV1.8-expressing mouse nociceptors, identifying 353 transcripts and 78 proteins, and finds moderate correlation between proteome and transcriptome datasets.

This study examines age and sex differences in opioid receptor signaling in the vlPAG of rats, finding reduced receptor binding, G-protein activation, and cAMP inhibition in aged rats, along with increased RGS4 and RGS9-2 expression, which may explain reduced opioid potency in aging.

This study shows TNFα sensitizes colonic nociceptors via TNFR1 and p38 MAPK, enhancing responses to capsaicin and noxious distension.