Impaired thyroid function provoked by neonatal treatment with drugs affecting the maturation of monoaminergic and opioidergic neurons.

Abstract The aim of the present work was to study the basal secretion rate and the reactivity of the TSH-thyroid axis in adult rats neonatally exposed to drugs influencing monoaminergic and opioidergic neurons. The early postnatal administration of drugs antagonistic with the dopaminergic or serotoninergic neurons resulted in a persistent higher rate of basal secretion of TSH, while the administration of drugs synergistic with the monoaminergic neuron systems was weakly influential in this respect. The exposure to opioids in the perinatal period resulted in a permanent reduction of serum TSH levels which was even more pronounced when the exposure to morphine was advanced to the fetal period of life. These data raise the possibility that the permanent TSH depressing effect of perinatal administration of opioids is due to their effect exerted on the maturation of the monoaminergic neurons. From the other hand, our results lead to assume that there is a perinatal critical period in the maturation of monoaminergic neurons regulating TSH secretion in the adult age. In accordance with this assumption, the data obtained in rats bearing perinatal neurotoxic destruction of catecholaminergic neurons contribute to the concept that the disturbed maturation of monoaminergic neurons in the supposed critical period of development might lead to permanent deficiency also in the reactivity of the TSH-thyroid axis.