Catecolaminergic systems and hypothalamic-pituitary-thyroid (HPT) axis: adrenaline, noradrenaline and dopamine treatments in vivo in lizard Podarcis siculus
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Updated: Sep 11, 2025

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Published on: May 12, 2019
Rosaria Sciarrillo1, Alessandra Falzarano1, Vito Gallicchio2
1Department of Science and Technologies, University of Sannio, Via F. de Sanctis snc, 82100 Benevento, Italy.
Abstract:
The catecolaminergic system, which uses dopamine, noradrenaline and adrenaline as neurotransmitters, originates in the brainstem nuclei and spreads widely throughout the central nervous system (CNS). Although there are data indicating that interactions between the catecolaminergic systems of the nervous system and hypothalamic-pituitary-thyroid axis do indeed take place and may be of physiological and clinical relevance, such interactions are far from being clarified. In this paper, we studied the hypothalamic-pituitary-thyroid axis responses in lizards treated with adrenaline, noradrenaline and dopamine respectively. Adrenaline raised plasma TRH and TSH levels and induced a stimulatory effect on the thyroid gland activity with an increase of T3 and T4 levels. On the contrary, noradrenaline treatment induced a reduction in TRH secretion, accompanied by a normal circulating TSH level and increased plasma T4 levels but with a reduction of circulating T3 levels. Dopamine stimulated TRH secretion centrally but induced TSH deficiency followed by reduction of circulating T3 and T4 levels. Furthermore, the effects of the catecolaminergic system on the TRH-TSH-thyroid hormone axis has been also manifested through mechanisms in peripheral organs such as the liver. The dynamic interplay between TRH and TSH and the feedback effects on circulating thyroid hormones after treatment with adrenaline, noradrenaline and dopamine is a very sophisticated and complicated mechanism that responds via afferent inputs from neurons originating in the paraventricular nucleus and can influence the secretion of TRH and TSH-secreting hypophysiotropic neurons with consequent feedback on thyroid hormones.
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