Scanned optogenetic control of mammalian somatosensory input to map input-specific behavioral outputs.

Somatosensory stimuli guide and shape behavior, from immediate protective reflexes to longer-term learning and higher-order processes related to pain and touch. However, somatosensory inputs are challenging to control in awake mammals due to the diversity and nature of contact stimuli. Application of cutaneous stimuli is currently limited to relatively imprecise methods as well as subjective behavioral measures.

Pain sensitivity and vasopressin analgesia are mediated by a gene-sex-environment interaction.

Quantitative trait locus mapping of chemical/inflammatory pain in the mouse identified the Avpr1a gene, which encodes the vasopressin-1A receptor (V1AR), as being responsible for strain-dependent pain sensitivity to formalin and capsaicin. A genetic association study in humans revealed the influence of a single nucleotide polymorphism (rs10877969) in AVPR1A on capsaicin pain levels, but only in male subjects reporting stress at the time of testing. The analgesic efficacy of the vasopressin analog desmopressin revealed a similar interaction between the drug and acute stress, as desmopressin inhibition of capsaicin pain was only observed in nonstressed subjects.

Distribution and identity of neurons expressing the oxytocin receptor in the mouse spinal cord.

Oxytocin can influence various spinal functions. However, little is known about the spinal neuronal networks responsible for oxytocin effects. The aim of this study was to localize and characterize spinal neurons expressing oxytocin receptors.

Oxytocin-induced analgesia and scratching are mediated by the vasopressin-1A receptor in the mouse.

The neuropeptides oxytocin (OXT) and arginine vasopressin (AVP) contribute to the regulation of diverse cognitive and physiological functions including nociception. Indeed, OXT has been reported to be analgesic when administered directly into the brain, the spinal cord, or systemically. Here, we characterized the phenotype of oxytocin receptor (OTR) and vasopressin-1A receptor (V1AR) null mutant mice in a battery of pain assays.