Role of Postnatal Gonadal Function in the Determination of Thyrotropin (TSH) Releasing Hormone-Induced TSH Response in Adult Male and Female Rats

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Abstract
Permanent effects of postnatal gonadal function on the hypothalamo-pituitary-thyroid axis were examined in male and female rats of the Wistar-Imamichi strain. Animals were used at the age of about 10 weeks. Neonatally castrated (NC) males showed a significantly higher plasma TSH response to TRH (10 .mu.g/kg BW, ip) than males castrated at 1, 2, 3, 4, or 6 weeks of age. The TSH response in intact males was similar to that seen in NC males. Neonatal androgenization of NC males with 100 .mu.g/rat of testosterone propionate decreased the TSH response in the group. The anterior pituitary (AP) TSH content was similar among all male groups. The number of AP TRH receptors was significantly higher in both NC males and intact males than in both NC + neonatal androgenization males and 6-week-castrated males. In female rats, TRH-induced TSH response, AP TSH content, and AP TRH receptor number were all unaffected by the age of castration, whereas intact females significantly exceeded 6-week-castrated females in these three variables. The circulating levels of T3 and T4 and hypothalamic TRH content were similar in all groups in each sex. These results indicate biphasic effects of postnatal testosterone on the TSH response to TRH, that is, a permanent inhibition in early postnatal days and a transient stimulation in adult age. The effects occurred not via changes in AP TSH content but via changes in AP TRH receptor number. In females, however, postnatal gonads did not exert any permanent effects on the TRH-TSH systems.