Laboratorio de Neurobiología, Instituto de Embriología e Histología (IHEM-CONICET), Facultad de Ciencias Médicas, Universidad Nacional de Cuyo (UNCuyo), 5500, Mendoza, Argentina; Laboratorio de Ciencias Fisiológicas, Cátedra de Bacteriología y Virología Médicas, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, 5000, Córdoba, Argentina.
Laboratorio de Reproducción y Lactancia, Instituto de Medicina y Biología Experimental de Cuyo (IMBECU-CONICET), Centro Científico Tecnológico (CCT), 5500, Mendoza, Argentina; Facultad de Ciencias Exactas y Naturales, UNCuyo, 5500, Mendoza, Argentina.
Peptides. 2019 Mar;113:1-10. doi: 10.1016/j.peptides.2018.12.008. Epub 2018 Dec 24.
The Neuropeptide EI (NEI, glutamic acid- isoleucine amide) participates in neuroendocrine function. Previously we demonstrated that NEI concentration is regulated by thyroid hormones in discrete hypothalamic areas in rats. We observed that the thyroid status affects the dopaminergic regulation of the pituitary hormones. In this study we explored possible interactions between NEI and tyrosine hydroxylase (TH) containing elements in selected hypothalamic areas of male rats. Neuronal somas, terminals and boutons were assessed by confocal microscopy, in hypo- and hyperthyroid animals. We observed a remodeling of the contacts between the TH and NEI immunoreactive elements in the incerto-hypothalamic area (IHy, also known as rostromedial zona incerta) according to thyroid function. However, in the dorsolateral zone of the peduncular part of the lateral hypothalamus (DL-PLH) the thyroid hormones affect the dendritic trees of the neurons without perturbing the overall NEI/TH contacts. Also, we demonstrated that TRH Receptor 1 (TRH-R1) is colocalized in NEI immunoreactive neurons in the peduncular part of the lateral hypothalamus (PLH) and NEI precursor mRNA expression increased by hypothyroidism indicating that NEI neurons are responsive to the feedback mechanisms of the Hypothalamic Pituitary-Thyroid Axis (HPT). In conclusion, the hypothyroid status seems to increase the interactions between the NEI neurons and the dopaminergic pathways while hyperthyroidism either decreases or displays no effects. Altogether these observations support the participation of the IHy and PLH NEI as a modulating component of the HPT suggesting that altered neuroendocrine, behavioral and cognitive dysfunctions induced by dysthyroidism could be in part mediated by NEI.
神经肽 EI（NEI，谷氨酸-异亮氨酸酰胺）参与神经内分泌功能。我们之前的研究表明，NEI 浓度受甲状腺激素在大鼠离散下丘脑区域的调节。我们观察到甲状腺状态会影响垂体激素的多巴胺调节。在这项研究中，我们探索了 NEI 与选定的雄性大鼠下丘脑区域中含酪氨酸羟化酶（TH）的元素之间可能存在的相互作用。在甲状腺功能减退和甲状腺功能亢进的动物中，通过共聚焦显微镜评估神经元体、末梢和末梢小体。我们观察到，根据甲状腺功能，TH 和 NEI 免疫反应性元素之间的接触发生了重塑，在中脑-下丘脑区域（IHy，也称为前内侧未定带）中。然而，在外侧下丘脑的被盖脚部分的背外侧区（DL-PLH）中，甲状腺激素影响神经元的树突而不干扰 NEI/TH 接触的整体。此外，我们还证明，促甲状腺激素释放激素受体 1（TRH-R1）在外侧下丘脑的被盖脚部分（PLH）的 NEI 免疫反应性神经元中与 TRH-R1 共定位，并且甲状腺功能减退症可增加 NEI 前体 mRNA 的表达，表明 NEI 神经元对下丘脑-垂体-甲状腺轴（HPT）的反馈机制有反应。总之，甲状腺功能减退症似乎增加了 NEI 神经元与多巴胺能通路之间的相互作用，而甲状腺功能亢进症则减少或不显示任何影响。总的来说，这些观察结果支持 IHy 和 PLH 的 NEI 作为 HPT 的调节成分参与，这表明甲状腺功能障碍引起的神经内分泌、行为和认知功能障碍可能部分由 NEI 介导。
