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Altered growth hormone and prolactin responsiveness to TRH in the infant rat
Insights
Thyrotropin-releasing hormone (TRH) increases growth hormone (GH) in infant rats, but prolactin (PRL) release is limited. Central sympathectomy with 6-hydroxydopamine (6-OHDA) further disrupts these responses, suggesting a developing central nervous system-anterior pituitary connection.
Area of Science:
- Endocrinology
- Neuroscience
- Developmental Biology
Background:
- Thyrotropin-releasing hormone (TRH) is a key regulator of anterior pituitary hormone secretion.
- The developmental neuroendocrine axis, particularly the interaction between the central nervous system (CNS) and anterior pituitary (AP), is complex and undergoes significant changes.
- Understanding the differential responsiveness of growth hormone (GH) and prolactin (PRL) to TRH during development is crucial for comprehending pituitary function.
Purpose of the Study:
- To investigate the effects of TRH on plasma GH and PRL levels in infant rats.
- To examine the role of the central sympathetic nervous system, using 6-hydroxydopamine (6-OHDA), in mediating TRH-induced hormone release.
- To explore the developmental changes in CNS-AP communication influencing pituitary hormone responses.
Main Methods:
- Radioimmunoassay (RIA) was used to measure plasma GH and PRL levels in 12-day-old male and female rat pups.
- TRH was administered intraperitoneally at various doses.
- Central sympathectomy was performed using intraventricular 6-OHDA one week prior to hormone level assessment.
Main Results:
- TRH significantly increased plasma GH levels in a non-dose-related manner across tested doses.
- TRH stimulated PRL release only at the highest dose (1.5 mug/100 g b.w.).
- Central sympathectomy with 6-OHDA abolished TRH-induced PRL release and diminished GH responsiveness, while increasing baseline PRL and reducing GH response to insulin hypoglycemia and cold stress.
Conclusions:
- Infant rats exhibit a greater GH than PRL responsiveness to TRH compared to adult patterns, suggesting a developing CNS-AP connection.
- Central sympathectomy by 6-OHDA further impairs TRH-induced PRL release and alters GH regulation, supporting the hypothesis of a physiologically functional disconnection in the infant rat.
- These findings highlight the dynamic maturation of the neuroendocrine system and its impact on pituitary hormone regulation during early development.
Abstract:
12-day-old female and male pups were killed 10 min after the injection of either saline or thyrotropin releasing hormone (TRH), and plasma growth hormone (GH) and prolactin (PRL) levels were measured by radioimmunoassay (RIA). At all doses used (0.15, 0.3, 0.6 and 1.5 mug/100 g b.w.i.p.), TRH induced a significant, although not dose-related, increase in plasma GH levels, but was effective in releasing PRL only at the greatest dose level (1.5 mug/100 g b.w.). The GH-releasing effect of TRH was even more evident in 12-day-old pups subjected to central sympathectomy of 6-hydroxydopamine (6-OHDA, 60 mug/10 mul intraventricular route) 1 week before; in these animals, TRH was ineffective in releasing PRL even at the greatest dose level (1.5 mug/100 g b.w.). In pups pretreated with 6-OHDA, the GH-lowering effect of insulin hypoglycemia or cold exposure was markedly reduced, while the PRL responses were unmodified. Baseline plasma PRL levels were markedly increased following 6-OHDA administration. It is proposed that in the infant rat the greater GH than PRL responsiveness to TRH, which opposed the pattern of response present in the adult animal, may be due to the existence of a 'physiologic' functional disconnection between the central nervous system (CNS) and the anterior pituitary (AP). Results obtained following central sympathectomy by 6-OHDA, which further disrupted CNS-AP links, substantiate this view.