Central administration of prostaglandin E2 (PGE2) is associated with potent anorexia in rodents and chicks, although hypothalamic mechanisms are not fully understood. The objective of the present study was to identify hypothalamic nuclei and appetite-related factors that are involved in this anorexigenic effect, using chickens as a model. Intracerebroventricular injection of 2.5, 5, and 10 nmol of PGE2 suppressed food and water intake in broiler chicks in a dose-dependent manner. c-Fos immunoreactivity was increased in the paraventricular nucleus (PVN) at 60 min post injection of 5 nmol of PGE2. Under the same treatment condition, hypothalamic expression of melanocortin receptor 3 and ghrelin mRNAs increased, whereas neuropeptide Y receptor sub-type 5 and tropomyosin receptor kinase B (TrkB) mRNAs decreased in PGE2-treated chicks. In the PVN, chicks injected with PGE2 had more brain-derived neurotrophic factor (BDNF), ghrelin, and c-Fos mRNA but less corticotrophin-releasing factor receptor 1 (CRFR1), CRFR2, and TrkB mRNA expression. In conclusion, PGE2 injection resulted in decreased food and water intake that likely involves BDNF and ghrelin originating in the PVN. Because the anorexigenic effect is so potent and hypothalamic mechanisms are similar in chickens and rodents, a greater understanding of the role of PGE2 in acute appetite regulation may have implications for treating eating and metabolic disorders in humans.

尽管下丘脑机制尚不完全清楚，但前列腺素 E2 (PGE2) 的中枢给药与啮齿动物和雏鸡的严重厌食症有关。本研究的目的是以鸡为模型，确定参与这种厌食效应的下丘脑核团和食欲相关因素。脑室内注射 2.5、5 和 10 nmol PGE2 以剂量依赖性方式抑制肉鸡的食物和水摄入。注射 5 nmol PGE2 后 60 分钟，室旁核 (PVN) 中的 c-Fos 免疫反应性增加。在相同的处理条件下，PGE2 处理的雏鸡下丘脑黑皮质素受体 3 和生长素释放肽 mRNA 的表达增加，而神经肽 Y 受体亚型 5 和原肌球蛋白受体激酶 B (TrkB) mRNA 的表达减少。在PVN中，注射PGE2的雏鸡具有更多的脑源性神经营养因子（BDNF）、生长素释放肽和c-Fos mRNA表达，但促肾上腺皮质激素释放因子受体1（CRFR1）、CRFR2和TrkB mRNA表达较少。总之，注射 PGE2 导致食物和水摄入量减少，这可能与源自 PVN 的 BDNF 和生长素释放肽有关。由于厌食作用非常有效，而且鸡和啮齿动物的下丘脑机制相似，因此更好地了解 PGE2 在急性食欲调节中的作用可能对治疗人类饮食和代谢紊乱具有重要意义。