Pancreatic polypeptide and peptide YY3–36 induce Ca2+ signaling in nodose ganglion neurons

• Published in: Neuropeptides (Edinburgh) 2013-02, Vol.47 (1), p.19-23
• Main Authors: Iwasaki, Yusaku, Kakei, Masafumi, Nakabayashi, Hajime, Ayush, Enkh-Amar, Hirano-Kodaira, Misato, Maejima, Yuko, Yada, Toshihiko
• Format: Article
• Language: English
• Subjects: Advanced Basic Science; Animals; Calcium Signaling - drug effects; Capsaicin - pharmacology; Cytosolic Ca2; Eating - physiology; Endocrinology & Metabolism; Feeding; Humans; In Vitro Techniques; Male; Mice; Mice, Inbred ICR; Neurons - drug effects; Neurons, Afferent - drug effects; Neuropeptide Y - pharmacology; Nodose ganglion; Nodose Ganglion - cytology; Nodose Ganglion - drug effects; Pancreatic polypeptide; Pancreatic Polypeptide - pharmacology; Peptide Fragments - pharmacology; Peptide YY; Peptide YY - pharmacology; Potassium Chloride - pharmacology; Rats; Sincalide - metabolism; Vagal afferent nerves; Vagus Nerve - cytology; Vagus Nerve - drug effects
• ISSN: 0143-4179; 1532-2785
• DOI: 10.1016/j.npep.2012.07.006

Abstract Peripheral injection of pancreatic polypeptide (PP) and peptide YY3–36 (PYY3–36 ), the hormones released in response to meals, reduce food intake, in which the rank order of the potency is PP > PYY3–36 . These anorectic effects are abolished in abdominal vagotomized rats, suggesting that PP and PYY3–36 induce anorexia via vagal afferent nerves. However, it is not clear whether PP and PYY3–36 directly act on vagal afferent neurons. In this study, we examined the effects of PP and PYY3–36 on cytosolic Ca2+ concentration ([Ca2+ ]i ) in isolated nodose ganglion neurons of the mouse vagal afferent nerves. At 10−11 M, PP but not PYY3–36 recruited a significant population of nodose ganglion neurons into [Ca2+ ]i increases. PP at 10−11 to 10−7 and PYY3–36 at 10−10 to 10−7 M increased [Ca2+ ]i in a concentration-dependent manner. At submaximal to maximal concentrations of 10−10 and 10−8 M, PP increased [Ca2+ ]i in approximately twice greater population of nodose ganglion neurons than PYY3–36 . Furthermore, the majority of PP-responsive neurons also exhibited [Ca2+ ]i responses to cholecystokinin-8, a hormone known to induce satiety through activating nodose ganglion neurons. The results demonstrate that PP and PYY3–36 directly activate nodose ganglion neurons and suggest that the marked effect of PP on cholecystokinin-8-responsive nodose ganglion neurons could be linked to the regulation of feeding.