In order to reveal the action of gonadotropin-releasing hormone (GnRH) on the synthesis of gonadotropins in the pituitary gland of castrated rats, passive immunization to GnRH designed to block the activity of GnRH was performed. The levels of prolactin mRNA in castrated and rabbit anti-GnRH serum (RAGnRH)-treated rats decreased, whereas TSH beta mRNA showed no statistically significant change. In contrast, mRNAs encoding common alpha, LH beta and FSH beta were increased 2.7-, 1.7- and 1.5-fold, respectively, by castration. These elevated mRNA levels of gonadotropin subunits in castrated rats well explain the increased hormone levels in serum and in the pituitary. Two days later, a single administration of RAGnRH to the castrated rats significantly suppressed the mRNA levels to 2.0-fold for alpha, 1.2-fold for LH beta and 1.1-fold for FSH beta relative to the respective control values. These results showed that the two gonadotropin beta genes respond more rapidly to GnRH action that the common alpha gene.