In goldfish GH transiently rises 30 minutes after meals returning to the baseline at one hour post-meal. Somatostatin (SRIF) is the major inhibitor of GH release. Three cDNAs encoding pre-pro-SRIF (PSS) have been previously cloned from goldfish brain; PSS-I encoding SRIF-14, PSS-II potentially processed into gSRIF-28 that has [Glu¹, Tyr⁷, Gly¹⁰] SRIF-14 at the C-terminus, and PSS-III that encodes [Pro²] SRIF-14 at its C-terminus. In goldfish, bombesin (BBS), mimicking the endogenous gastrin releasing peptide (GRP), acutely suppresses food intake and also stimulates GH release. Ghrelin was recently characterized in goldfish as a GH secretagogue and an orexigen. In this paper, we studied the changes in SRIF mRNA levels during feeding and analyzed the influences of BBS and ghrelin peptides on forebrain PSS expression. The results showed a 60% reduction in PSS-II mRNA after meals, but no changes in the expression of PSS-I and -III were found. Intraperitoneal (ip) injections of 100 ng/g body weight (BW) of BBS increased GH secretion and decreased PSS-I and -II gene expression. Ip injection of goldfish ghrelin (100 ng/g BW) transiently increased the serum GH levels, and increased PSS-I while decreasing PSS-II mRNA levels. Ghrelin (50 ng/g BW) blocked the effects of BBS (100 ng/g BW) on the expression of PSS-I but not on PSS-II. Co-administration of BBS and ghrelin decreases only the PSS-II gene expression. We conclude that the interactions between BBS/GRP and ghrelin can account for the post-prandial variations in serum GH levels and the forebrain expression of PSS-II. Furthermore, we demonstrated that ip administration of BBS reduces the ghrelin expression levels in the gut. Thus, the inhibition of production of ghrelin in the gut may contribute to the satiety effects of BBS/GRP peptides.