Kisspeptin-10 elicits triphasic cytosolic calcium responses in immortalized GT1-7 GnRH neurones

Ozcan M., Alcin E., AYAR A., Yilmaz B., SANDAL S., Kelestimur H.

NEUROSCIENCE LETTERS, vol.492, no.1, pp.55-58, 2011 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 492 Issue: 1
  • Publication Date: 2011
  • Doi Number: 10.1016/j.neulet.2011.01.054
  • Journal Name: NEUROSCIENCE LETTERS
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.55-58
  • Keywords: Kisspeptin-10, Calcium signaling, GT1-7 cells, GONADOTROPIN-RELEASING-HORMONE, PROTEIN-COUPLED-RECEPTOR, EXPRESSION, KISS-1, GPR54, GENE, SYSTEM
  • Karadeniz Technical University Affiliated: Yes

Abstract

Kisspeptins, which are alternatively called as metastin since they were originally identified as products of metastasis suppressor gene KiSS-1, are the natural ligands for the G protein-coupled receptor 54 (GPR54). Kisspeptins are the most potent activators of hypothalamic-pituitary-gonadal (HPG) axis reported to date. The pulsatile pattern of GnRH release, which results in the intermittent release of gonadotropic hormones from the pituitary, has a critical importance for reproductive function but the factors responsible from this release pattern are not known. Therefore, the pattern of kisspeptin-induced intracellular signaling and the role of PKC in the intracellular signaling cascade were investigated by fluorescence calcium imaging using the immortalized GnRH-secreting GT1-7 hypothalamic neurons. Kisspeptin-10 caused a triphasic change characterized by an initial small increase followed by a significant decrease and increase in intracellular free calcium concentrations ([Ca2+](i)). The changes in [Ca2+](i) were significantly attenuated by pre-treatment with protein kinase C inhibitor. The compatibility of appeared mirrored-patterns of kisspeptin-10-induced changes in [Ca2+](i) concentrations in these neurons and GnRH secretion confirm the importance of intracellular calcium flux downstream from GPR54 through PKC signaling pathway. (C) 2011 Elsevier Ireland Ltd. All rights reserved.