Pain Mechanisms and Treatments

This study investigates if temporal pain contrast enhancement can be induced by repetitive stimulation with different interstimulus intervals and finds it occurs for 5 and 15 seconds but not 25 seconds.

The paper uses machine learning to analyze single-trial laser evoked potentials (LEPs) in rats, identifying distinct Aδ- and C-fibre mediated responses that predict pain behavior.

The paper uses microarray analysis to identify potential biomarkers for neuropathic pain after brachial plexus avulsion by comparing gene expression in pain and control groups.

This study evaluates the analgesic and neuroprotective effects of etifoxine in a mouse model of diabetic neuropathy, showing reduced mechanical hyperalgesia and anxiety.

This study finds no difference in pain sensitivity between obese and healthy weight individuals, suggesting obesity may not increase susceptibility to chronic pain through heightened nociception.

This study investigates the role of SUR1-subtype KATP channels in opioid-induced antinociception and hyperlocomotion, finding attenuated antinociception and potentiated hyperlocomotion in SUR1-deficient mice.

The paper identifies molecularly diverse spinal and trigeminal projection neurons involved in pain and itch, revealing distinct subsets and their functional roles.

The paper investigates whether affective or cognitive processes drive cortical encoding of pain, finding a stronger link between cortical data and unpleasantness ratings than intensity ratings.

This study shows miR-135-5p reduces bone cancer pain in mice by inhibiting astrocyte inflammation and the JAK2/STAT3 pathway.

This study shows that microglial ablation does not impair opioid-induced hyperalgesia in rodents, challenging the assumption of microglial involvement in this condition.

This study shows that a high ω-6 PUFA diet causes reversible peripheral nerve dysfunction and worsens pain in mice, with potential therapeutic implications.

The paper maps behavioral signatures of inflammatory pain and its relief in mice using computational tools and identifies that a common anti-inflammatory drug does not fully restore pre-injury behavior.

This study shows that spinal cord injury rapidly alters nociceptor response properties, leading to increased sensitivity and spontaneous activity, contributing to chronic pain.

This study shows that CRF neurons in the BNST differently influence pain processing and modulation in male and female mice, with CRF being necessary for pain behaviors.

The paper uses scRNA-seq to identify cell-type-specific transcriptional changes in the retrosplenial cortex after nerve injury, revealing an excitatory/inhibitory synaptic imbalance linked to pain hypersensitivity.

The paper shows that hypoxia in the spinal dorsal horn, caused by vascular issues, activates sensory neurons and leads to neuropathic pain, which can be reversed by inhibiting carbonic anhydrase.

This study shows capsaicin pretreatment reduces postoperative pain by decreasing Ca2+ activity in primary sensory neurons and degenerating nerve fibers in the skin.

The paper investigates how spinal cord networks in mice encode inflammatory hyperalgesia through changes in neuronal activity and synaptic inhibition.

The paper identifies transcriptomic and epigenetic changes in rat dorsal root ganglia under two chronic pain models, revealing shared and distinct chromatin accessibility alterations.

This study shows that adolescent restraint stress in rats leads to long-term spinal neuron sensitization, which is further enhanced by a mild-nociceptive input in adulthood.

This study identifies a novel mechanism by which astrogliosis contributes to HIV-associated pain through Wnt5a signaling and IL-1β regulation.

The paper investigates how growth hormone signaling in the periphery modulates neonatal nociception, finding that GH receptor signaling inhibits hypersensitivity and that injury disrupts this by sequestering GH via macrophages.

The paper identifies a distinct nociresponsive region in mouse primary somatosensory cortex that processes nociceptive input separately from tactile input.

This study investigates the role of artemin/GFRα3 signaling in osteoarthritis pain using mouse models and finds that blocking this signaling reduces hypersensitivity and improves limb use.

The paper characterizes firing patterns of Y1eGFP neurons in the spinal cord and finds they exhibit delayed short-latency firing under hyperpolarized conditions, associated with fast A-type potassium currents and T-type calcium channel activity.

This study uses ASL to image neural correlates of parametrically modulated mechanical pain in healthy humans, identifying brain regions and perfusion dynamics associated with pain intensity and force.

This study shows that increased NALCN expression contributes to neuropathic pain and suggests NALCN as a potential therapeutic target.

This study shows that optogenetic activation of spinal microglia in mice induces chronic pain through IL-1 signaling and increased neuronal activity.

This study investigates the role of β-arrestin-2 in opioid tolerance in dorsal root ganglia neurons, finding it mediates acute but not chronic tolerance.

The paper identifies primate sensory neuron types associated with human chronic pain using transcriptomics and maps human pain heritability to these neuronal types.