Statistical learning shapes pain perception by allowing the brain to predict and modulate pain intensity based on temporal patterns, providing insights into pain regulation and their relevance to chronic pain.

Constitutive sphingosine 1-phosphate signaling via the G-protein coupled receptor S1PR3 in mechanonociceptive somatosensory neurons is required for normal behavioral responses to noxious mechanical stimuli.

An interdisciplinary approach uncovers a new antinociceptive molecular mechanism and shows that the adhesion GPCR CIRL adjusts the sensation of gentle touch and noxious mechanical insult in opposite directions.

Regulatory T cells produce analgesic opioid peptides that limit heat sensitivity in mice, revealing a novel pain regulation mechanism independent of inflammation control.

Through associative learning, environmental context can come to exert control over the endogenous opioid system such that it is recruited as a conditioned compensatory response to ongoing painful stimuli in both male and female mice, or in anticipation of a painful stimulus in females.

Localized drug photoactivation provides light-mediated analgesia in behaving mice.

Single-cell RNA-sequencing unraveled cell subtype-specific transcriptomic changes in both injured and uninjured primary sensory neurons after nerve injury and demonstrated transcriptomic sexual dimorphism.

Exogenous opioid analgesia is mediated by MORs expressed in glutamatergic neurons, whereas endogenous opioid analgesia is mediated by MORs expressed in GABAergic neurons.

Attention-grabbing tasks produce rapid opioid-mediated analgesia via the descending pain modulation network to alter spinal neuronal activity.

Cells utilize a membrane-mediated mechanism for mechanosensation, which involves the disruption of lipid rafts and a signal relayed to an ion channel.