To study the role of IGF-I on GH secretion, we looked firstly for IGF-I binding sites in the central nervous system. IGF-I presents a single class of binding sites on brain membranes and pituitary extracts. Their affinity constants (Ka) were 11.44 +/- 4.66 and 4.42 +/- 1.37 x 10(9) M-1, respectively and their capacity (Bmax) were 119.83 +/- 46.21 and 73.65 +/- 20.87 fmoles/mg, respectively. In a second step IGF-I and bGH action on GH release was tested in vitro and in vivo. IGF-I inhibited GH release by pituitary cell cultures while bGH did not, suggesting direct action of IGF at the pituitary level and indirect action of GH, possibly mediated by IGF-I. IGF-I injected into catheterization fish induced a rapid inhibition of GH release, while bGH induced a delayed one. This timing supports a direct effect of IGF-I on GH release and the indirect effect of bGH. So peripheral IGF-I can play a role on GH secretion, perhaps as a mediator of GH action. This could explain the delayed fluctuation of GH and IGF-I plasma levels previously observed. This strong relationship between plasma IGF and GH secretion in trout seems to be different from that in mammals in which systemic IGF does not seem to play a predominant role in regulating GH secretion.