Aiming to elucidate the role of GH and IGF-I with regard to vertebral and white muscle growth, gene expression of the GH and IGF-I receptors (ghr and igf-Ir, respectively) and local IGF-I (igf-I) were analyzed during spring growth (January-June) in Atlantic salmon postsmolts. One group of fish was reared under natural light (NL), while one group was reared under continuous light (LL). Growth rate of fork length was higher in the LL group for a short period after onset of continuous light (LL: 0.50+/-0.02 mm day(-1), NL: 0.43+/-0.01 mm day(-1)) and for a longer period at the end of the experiment in June (LL: 1.18+/-0.06 mm day(-1), NL: 0.75+/-0.02 mm day(-1)). Likewise, growth rate in length of vertebra No. 40 in the LL group was higher than in the NL group the first period after onset of light (LL: 0.015+/-0.002 mm day(-1), NL: 0.008+/-0.001 mm day(-1)). Plasma GH levels peaked in late February and were higher in the LL group than in the NL group (LL: 7.27+/-0.61 ng ml(-1), NL: 2.60+/-0.50 ng ml(-1)), whereas plasma IGF-I levels peaked in early February and were unaffected by photoperiod. ghr expression was upregulated in late February in liver (12-fold), white muscle (6-fold) and vertebral tissue (3-fold) and higher in the LL group than in the NL group (2-fold) in vertebral tissue in late March. White muscle expression of igf-I and igf-Ir decreased from initial levels throughout the experiment. Hepatic gene expression of igf-I doubled in both groups in late February, followed by a 4-fold upregulation in June in the LL group only. Vertebral tissue expression of igf-I (4-fold) and igf-Ir (6-fold) increased in May and were unaffected by photoperiod. One exception was a smaller upregulation of igf-I (2-fold) in the LL group in early February. In conclusion, GH appears to have an initial role in stimulating vertebral growth, while IGF-I seems to stimulate growth during late spring. It is suggested that local IGF-I acts as a paracrine agent, evaluated from the concurrent upregulation of igf-I and igf-Ir. The upregulation of ghr in white muscle tissue, concurrent with a downregulation of muscle igf-I and igf-Ir, indicate that GH stimulated growth or metabolism independent of IGF-I.