clinical and experimental studies indicate a role for GH in mechanisms rela
ted to anhedonia/hedonia, psychic energy, and reward. Recently we showed th
at transgenic mice with general overexpression of bovine GH display increas
ed spontaneous locomotor activity. In the present study, we investigated wh
ether this behavioral change is owing to a direct action of GH in the centr
al nervous system or to peripheral GH actions. A transgenic construct, cont
aining the glial fibrillary acidic protein promoter directing specific expr
ession of bovine GH to the central nervous system, was designed. The centra
l nervous system-specific expression of bovine GH in the glial fibrillary a
cidic protein-bovine GH transgenic mice was confirmed, but no effect on spo
ntaneous locomotor activity was observed. Serum bovine GH levels were incre
ased in glial fibrillary acidic protein-bovine GH transgenic mice but clear
ly lower than in transgenic mice with general overexpression of bovine GH.
In contrast to the transgenic mice with general overexpression. of bovine G
H, glial fibrillary acidic protein-bovine GH mice did not display any diffe
rence in serum IGF-I levels. The levels of free T-3 and the conversion of t
he free T-4 to free T-3 were only increased in transgenic mice with general
overexpression. of bovine GH, but serum corticosterone levels were similar
ly increased in both transgenic models. These results suggest that free T-3
and/or IGF-I, affecting dopamine and serotonin systems in the central nerv
ous system, may mediate the enhanced locomotor activity observed in transge
nic mice with general overexpression of bovine GH.