Departamento de Genética del Desarrollo y Fisiología Molecular, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Av. Universidad 2001, Cuernavaca, Mor. 62271, Mexico.
Brain Res. 2011 Jan 7;1367:188-97. doi: 10.1016/j.brainres.2010.10.011. Epub 2010 Oct 30.
Neurons of the paraventricular nuclei of the hypothalamus (PVN) that synthesize the peptide thyrotropin releasing hormone (TRH) control energy homeostasis. Identifying the circuits which regulate these neurons is critical to fully understand integration of metabolic information and the mechanisms that set thyroid hormone levels. We tested the hypothesis that nitric oxide (NO) acutely controls PVN TRH expression and thyrotropin (TSH) secretion by the anterior pituitary. The subcutaneous treatment of rats with N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthases, enhanced PVN TRH mRNA and medio-basal hypothalamic TRH levels, and reduced serum TSH concentration. Analysis of the effect of a NO donor in primary cultures of hypothalamic or anterior pituitary cells suggested that the effect of NO includes a direct action on hypothalamic neurons. The cold stress-induced increase in TSH release was inhibited by sc L-NAME. Therefore, production of NO may control the activity of the hypothalamus-pituitary-thyroid axis.
下丘脑室旁核（PVN）合成促甲状腺激素释放激素（TRH）的神经元控制着能量稳态。确定调节这些神经元的回路对于充分理解代谢信息的整合以及设定甲状腺激素水平的机制至关重要。我们测试了以下假设：即一氧化氮（NO）可急性控制 PVN 的 TRH 表达和垂体前叶的促甲状腺激素（TSH）分泌。用 N(G)-硝基-L-精氨酸甲酯（L-NAME）皮下治疗大鼠，这是一种一氧化氮合酶抑制剂，可增强 PVN 的 TRH mRNA 和中基底下丘脑 TRH 水平，并降低血清 TSH 浓度。对下丘脑或垂体前叶细胞原代培养物中 NO 供体作用的分析表明，NO 的作用包括对下丘脑神经元的直接作用。冷应激引起的 TSH 释放增加被 sc L-NAME 抑制。因此，NO 的产生可能控制着下丘脑-垂体-甲状腺轴的活性。
