title: Nesfatin-1 increases intracellular calcium concentration by protein kinase C activation in cultured rat dorsal root ganglion neurons.
abstract: Nesfatin-1 is a recently identified anorexigenic hypothalamic polypeptide derived from the posttranslational processing of nucleobindin 2 (NUCB2). Several studies have indicated that this neuropeptide may be participated in somatosensory and visceral transmission including pain signals in addition to energy metabolism. The aim of this study was to explore the possible role of nesfatin-1 in the transmission of peripheral neural signals by investigating the effects of nesfatin-1 on intracellular free calcium levels ([Ca(2+)]i) in cultured neonatal rat dorsal root ganglion (DRG) neurons. The effects of nesfatin-1 on [Ca(2+)]i in DRG neurons were investigated by using an in vitro calcium imaging system. DRG neurons were grown in primary culture following enzymatic and mechanical dissociation of ganglia from 1-or 2-day-old neonatal Wistar rats. Using the fura-2-based calcium imaging technique, the effects of nesfatin-1 on [Ca(2+)]i and role of the protein kinase C (PKC)-mediated pathway in nesfatin-1 effect were assessed. Nesfatin-1 elevated [Ca(2+)]i in cultured DRG neurons. The response was prevented by pretreating the cells with pertussis toxin. The protein kinase C inhibitor chelerythrine chloride suppressed nesfatin-1-induced rise in [Ca(2+)]i. The result shows that nesfatin-1 interacts with a G protein-coupled receptor, leading to an increase of [Ca(2+)]i, which is linked to protein kinase C activation in cultured rat DRG neurons.
authors.affiliation: Department of Biophysics, Faculty of Medicine, Firat University, Elazig, Turkey. Electronic address: meteozcan@hotmail.com.
authors.forename: Mete
authors.initials: M
authors.lastname: Ozcan
authors.affiliation: Department of Physiology, Faculty of Medicine, Firat University, Elazig, Turkey.
authors.forename: Zeynep Betul
authors.initials: ZB
authors.lastname: Gok
authors.affiliation: Department of Physiology, Faculty of Medicine, Firat University, Elazig, Turkey.
authors.forename: Emine
authors.initials: E
authors.lastname: Kacar
authors.affiliation: Department of Biophysics, Faculty of Medicine, Firat University, Elazig, Turkey.
authors.forename: Ihsan
authors.initials: I
authors.lastname: Serhatlioglu
authors.affiliation: Department of Physiology, Faculty of Medicine, Firat University, Elazig, Turkey.
authors.forename: Haluk
authors.initials: H
authors.lastname: Kelestimur
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000378:metabolism*; D002478:Cells, Cultured; D004268:DNA-Binding Proteins / Q000378:metabolism*; D004789:Enzyme Activation; D005727:Ganglia, Spinal / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D042541:Intracellular Space / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D000080866:Nucleobindins; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000378:metabolism*; D017208:Rats, Wistar; D011984:Sensory Receptor Cells / Q000187:drug effects* / Q000378:metabolism
chemical_list: D002135:Calcium-Binding Proteins; D004268:DNA-Binding Proteins; D009419:Nerve Tissue Proteins; C000630652:Nucb1 protein, rat; D000080866:Nucleobindins; D011493:Protein Kinase C; D002118:Calcium
keywords: Calcium signaling; G protein; Nesfatin; Pain; Protein kinase-C; Sensory neurons