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Updated: Feb 22, 2026

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Published on: March 12, 2019
Perinatal evolution and hormonal control of adrenal tyrosine hydroxylase activity in the rat
Insights
Adrenal tyrosine hydroxylase activity in fetal rats increases gradually, with a sharp rise after birth, likely due to birth stress. Adrenocorticotropic hormone (ACTH) directly influences this activity in fetal adrenal glands.
Area of Science:
- Developmental biology
- Neuroendocrinology
- Biochemistry
Background:
- Adrenal tyrosine hydroxylase (TH) is a key enzyme in catecholamine synthesis.
- Its developmental regulation in the perinatal period is not fully understood.
- Previous studies suggest hormonal and neural influences on TH activity.
Purpose of the Study:
- To investigate the developmental pattern of adrenal tyrosine hydroxylase activity in fetal and neonatal rats.
- To explore the roles of nervous mechanisms and hormones (ACTH, cortisol) in regulating this activity during the perinatal period.
Main Methods:
- Measurement of adrenal tyrosine hydroxylase activity in rat fetuses from 18.5 days of gestation to 24 hours postpartum.
- Surgical decapitation of fetuses to assess the role of the central nervous system.
- Administration of adrenocorticotropic hormone (ACTH) and cortisol to decapitated fetuses.
Main Results:
- Adrenal TH activity showed a gradual increase during fetal development, followed by a rapid, transient surge between 0-6 hours postpartum.
- Fetal decapitation significantly reduced term adrenal TH activity.
- Administration of ACTH partially restored TH activity in decapitated fetuses, while cortisol had no significant effect.
Conclusions:
- A nervous mechanism, possibly related to birth stress, contributes to the postpartum surge in adrenal TH activity.
- Adrenocorticotropic hormone (ACTH) exerts a direct regulatory effect on adrenal tyrosine hydroxylase activity in the fetal rat, similar to its action in adults.
Abstract:
The evolution of adrenal tyrosine hydroxylase activity has been measured in the rat fetus from 18 1/2 days of gestation until 24 h after birth. This activity increases gradually in the fetal adrenals with a sudden and transient increase between 0 and 6 h postpartum. It is suggested that a nervous mechanism related to the stress of birth is responsible for this increase. Fetal decapitation reduces adrenal tyrosine hydroxylase activity at term. This reduction can be partially prevented by administering adrenocorticotropic hormone (ACTH) to the decapitated fetus; cortisol administration has no effect. The results indicate that ACTH has a direct action on adrenal tyrosine hydroxylase in the fetus as it does in the adult.
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