Pain Mechanisms and Treatments

The paper characterizes MNK1 and MNK2 mRNA expression in human dorsal root and trigeminal ganglia, showing their expression in neurons and other cell types, supporting translational potential for pain-targeting therapies.

This study shows the PbN[->]CeA circuit contributes to injury-induced pain hypersensitivity but not baseline nociception in mice.

The paper identifies two functionally distinct serotonergic neuron populations in the hindbrain that have opposing effects on nociception by targeting different spinal regions.

The paper uses deep learning to analyze mouse behavior on a thermal-plate test to study pain hypersensitivity mechanisms.

The paper reports the expression of NaV1.7 mRNA and protein in specific neurons of the human spinal dorsal horn and discusses its potential role in pain phenotypes and analgesic efficacy.

The paper constructs a database of receptor-ligand pairs and uses single-cell transcriptomics to identify injury-specific neuroimmune interactomes in inflammatory pain.

This study investigates the neurochemical basis of pain relief modulation, finding that dopaminergic signaling, not opioidergic, enhances relief perception through active decision-making and unpredictability.

The paper investigates sex differences in pain behaviors following spinal cord injury in mice, finding that females exhibit heightened hypersensitivity compared to males.

This study shows pregabalin reduces cold allodynia caused by oxaliplatin by silencing specific sensory neurons through the 2{delta}-1 subunit of voltage-gated calcium channels.

This study shows that Orai1 channels regulate microglial reactivity and neuropathic pain, with sexual dimorphism observed in their effects.

The paper performs transcriptomic analysis of human dental biopsies to identify gene expression differences between symptomatic and asymptomatic patients and between sexes.

This study compares neurotransmitter levels in male and female mice after acute and chronic morphine treatment in specific brain regions, finding sex-based differences but limited effects of tolerance.

This study shows that activating β2-adrenergic receptors in microglia with Formoterol reduces neuropathic pain behaviors in mice by inhibiting microglial inflammation and structural changes.

The paper investigates short-latency nociceptive withdrawal reflex responses in humans and finds they are as painful as conventional latency responses, suggesting they may be mediated by ultrafast nociceptors.

The paper demonstrates that dorsal root ganglia (DRG) filter nociceptive signals through axonal t-junctions, with GABAergic cells enhancing this filtering and reducing pain hypersensitivity in models of inflammation and neuropathy.

The paper identifies neuronal loss in the secondary motor cortex as a mechanism underlying chronic neuropathic pain using longitudinal in vivo imaging.

This study identifies periosteal nerve sprouting and DRG metastasis in MM-induced bone pain, linking these changes to pain mechanisms and suggesting neuroprotective strategies.

The paper shows that newly repopulated spinal cord microglia have a unique transcriptome linked to pain resolution in a tibial fracture model.

The paper develops a novel mouse model of chronic primary pain conditions that mirrors human genetic, biological, and clinical features.

This study shows that activating mGlu4 receptors in the amygdala reduces neuropathic pain symptoms in mice, with differential effects based on the side of activation.

A selective androgen receptor modulator microparticle formulation alleviates widespread muscle pain in male and female mice while being non-toxic.

This study identifies Brn3a-positive spinal dorsal horn neurons as key contributors to visceral pain transmission in DSS-induced IBD mice, with a higher prevalence in spino-solitary projection neurons.

This study shows that spinal astrocytic glycogen dynamics, regulated by PTG, are critical for maintaining persistent pain through neuronal plasticity and metabolic coupling with neurons.

This study shows JMJD3 deficiency in midbrain dopamine neurons reduces dopamine levels and worsens chronic inflammatory pain.

This study shows that delta-opioid receptor agonists suppress itch while antagonists induce itch, revealing DOR's role in itch modulation in the spinal cord.

The paper shows inflammation causes a distal shift of the axon initial segment in inhibitory spinal cord neurons, reducing their excitability and contributing to pain.

This study investigates how descending inhibitory pathways affect HFS-induced hyperalgesia in humans and rats, finding that excitatory signaling outweighs inhibitory controls.

This study shows that Cav3.2 T-type calcium channels in the Anterior Pretectum are critical for neuropathic pain initiation and maintenance.

The paper shows that repetitive sensorimotor training and multimodal integration enhance neural plasticity, increasing stimulus-selectivity to nociceptive cues in healthy individuals.

The paper shows that vibrotactile touch reduces facial pain in mice by altering neural activity in the barrel cortex, integrating tactile and noxious signals.