Effects of cholecystokinin and bombesin on the expression of preprosomatostatin-encoding genes in goldfish forebrain

• Published in: Regulatory peptides Vol. 121; no. 1; pp. 99 - 105
• Main Authors: Canosa, Luis Fabián, Peter, Richard E
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 15-09-2004; Amsterdam Elsevier
• Subjects: Animals; Biological and medical sciences; Bombesin - administration & dosage; Bombesin - pharmacology; Cholecystokinin - administration & dosage; Cholecystokinin - pharmacology; Eating - drug effects; Food intake; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation - drug effects; Goldfish - genetics; Goldfish - metabolism; Growth hormone; Growth Hormone - blood; Growth Hormone - secretion; GRP; Prosencephalon - drug effects; Prosencephalon - metabolism; Protein Precursors - genetics; RNA, Messenger - genetics; RNA, Messenger - metabolism; Somatostatin - genetics; SRIF; Teleost fish; Vertebrates: endocrinology; SRIF; GRP; Growth hormone; Food intake; Teleost fish; Feeding behavior; Bombesin; Central nervous system; Somatotropin hormone; Neuropeptide; Prosencephalon; Gastrin releasing peptide; Vertebrata; Carassius auratus; Adenohypophyseal hormone; Gene; Pisces; Cholecystokinin; Hormone releasing factor
• ISSN: 0167-0115; 1873-1686
• DOI: 10.1016/j.regpep.2004.04.011

It was previously demonstrated that both cholecystokinin (CCK) and bombesin (BBS) stimulate growth hormone (GH) secretion in goldfish. Both peptides induce satiety and it was speculated that they integrate satiation and the postprandial increase in GH circulating levels. In the present paper we investigated the effects of CCK and BBS on the forebrain expression of the somatostatin gene family in goldfish to analyze if somatostatin peptides may be part of the effector mechanisms of CCK and BBS. We found that peripherally as well as centrally administered CCK decreases mRNA levels of preprosomatostatin (PSS)-I that encodes for SRIF-14, having no effects on PSS-II and PSS-III, which encode for gSRIF-28 and [Pro
2] SRIF-14, respectively. In addition, a direct action on the pituitary to stimulate GH release, this inhibition of PSS-I expression provides a possible mechanism for CCK to increase postprandial GH levels. On the other hand, BBS inhibits the forebrain expression of PSS-I and PSS-II but does not affect PSS-III regardless of the route of administration. We conclude that this could be the most likely mechanism of action of BBS to increase GH secretion, since there are few BBS-immunoreactive (IR) fibers and BBS binding sites in the anterior pituitary of goldfish.