Presence of oxytocin receptors in the gonadotrophin-releasing hormone (GnRH) neurones in female rats: a possible direct action of oxytocin on GnRH neurones.

نویسندگان

  • C S Caligioni
  • C Oliver
  • M C Jamur
  • C R Franci
چکیده

Gonadotrophin-releasing hormone (GnRH) neurones constitute the final output pathway of a neuronal network that controls the preovulatory luteinising hormone (LH) surge and ovulation. Throughout the reproductive cycle, several neurotransmitters stimulate and inhibit the activity of GnRH neurones, including oxytocin. The central administration of oxytocin antiserum abolishes the pro-oestrous LH surge whereas oxytocin stimulates GnRH secretion from hypothalamic explants suggesting an oxytocin central action. Within the GnRH neuronal population in the rat, GnRH cells in the medial preoptic area (MPOA) are activated at the time of the LH surge. Thus, we hypothesised that GnRH neurones in the MPOA may express oxytocin receptors, and that oxytocin neurones in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) may be differentially activated during the oestrous cycle. Oxytocin receptors mRNA was detected in the MPOA using reverse transcription-polymerase chain reaction. In animals in either metoestrus or pro-oestrus, double-label immunofluorescence indicated that approximately 10% of GnRH neurones in the MPOA coexpressed oxytocin receptors and that a few oxytocin fibres are located in the vicinity of these GnRH neurones. However, other neurones positive for the oxytocin receptors were found near GnRH neurones. At both oestrous stages, double-label immunofluorescence revealed that approximately 30% of oxytocin neurones in the SON were Fos-positive whereas oxytocin neurones in the PVN were consistently Fos-negative. Together, these data suggest that oxytocin may directly control neuronal activity in a subpopulation of GnRH neurones. Moreover, both oxytocin neuronal activity and the oxytocin receptor expression on GnRH cells are not influenced by oestrogen.

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عنوان ژورنال:
  • Journal of neuroendocrinology

دوره 19 6  شماره 

صفحات  -

تاریخ انتشار 2007