Oxytocin in hypothalamic supraoptic nucleus is transferred to the caudate nucleus to influence pain modulation

- Pain stimulation increased oxytocin concentration in CdN perfusion liquid.
- SON cauterization inhibited the oxytocin concentration increase in CdN perfusion liquid, which in both sides of SON cauterization was stronger than that in one side.
- SON microinjection of L-glutamate sodium increased oxytocin concentration in CdN perfusion liquid.
- CdN oxytocin came from SON during pain process.

Oxytocin (OXT), which is synthesized and secreted in the hypothalamic supraoptic nucleus (SON), is the most important bioactive substance in SON regulating pain process. Our previous study has pointed that OXT in the caudate nucleus (CdN) plays a role in pain modulation. The communication was designed to investigate the source of OXT in the rat CdN during pain process using the methods of push-pull perfusion and radioimmunoassay. The results showed that (1) pain stimulation increased the OXT concentration in the CdN perfusion liquid; (2) SON cauterization inhibited the increase of OXT concentration in CdN perfusion liquid induced by the pain stimulation, which role in both sides of SON cauterization was stronger than that in one side of SON cauterization; and (3) SON microinjection of l-glutamate sodium, which excited the SON neurons, increased OXT concentration in the CdN perfusion liquid. The data suggested that OXT in the CdN was influenced by SON during pain process, i.e., OXT in the SON might be transferred to the CdN to influence pain modulation.