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

Ludovic Wrobel, Ara Schorscher-Petcu, Anouk Dupré, Masahide Yoshida, Katsuhiko Nishimori, Eliane Tribollet

Research output: Contribution to journalArticlepeer-review

32 Citations (Scopus)


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. We used an oxytocin receptor-reporter mouse in which the fluorescent protein Venus is expressed under the control of the oxytocin receptor gene promoter. At all segmental levels, Venus-expressing neurons were most numerous in the substantia gelatinosa, mingled with protein kinase Cγ interneurons in the innermost layer of the inner lamina II, which, in contrast to the outer two thirds of this layer, does not receive nociceptive input. Venus-expressing neurons were also observed in the intermediolateral and sacral parasympathetic nuclei, where they represented about 5% of presumed preganglionic neurons identified by choline acetyltransferase immunoreactivity. Finally, Venus immunoreactivity was detected in lumbar and sacral dorsal gray commissures as well as in isolated neurons scattered in different regions of the dorsal horn. Altogether, our results establish the location of neurons putatively involved in oxytocin modulation of spinal functions, in particular of sexual functioning and nociception.

Original languageEnglish
Pages (from-to)49-54
Number of pages6
JournalNeuroscience Letters
Issue number1
Publication statusPublished - 2011 May 9


  • Autonomic system
  • Oxytocin receptor
  • Pain
  • Sacral dorsal gray commissure
  • Spinal cord
  • Substantia gelatinosa

ASJC Scopus subject areas

  • Neuroscience(all)


Dive into the research topics of 'Distribution and identity of neurons expressing the oxytocin receptor in the mouse spinal cord'. Together they form a unique fingerprint.

Cite this