Department of Physiology, Zanjan Branch, Islamic Azad University, Zanjan, Iran.
Division of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, University of Tehran, 14155-6453 Tehran, Iran.
Gen Comp Endocrinol. 2022 Jan 1;315:113930. doi: 10.1016/j.ygcen.2021.113930. Epub 2021 Oct 19.
Animal research indicates the neuropeptide Y (NPY), corticotrophin and melanocortin systems have a mediatory role in reward, however, how these substances interact with phenytoin-14 (PNX-14) induced food intake in birds remains to be identified. Accordingly, in this research eight tests were carried out to investigate the potential interactions of the NPY, melanocortin, as well as corticotrophin systems with PNX-14 on food consumption in neonatal chickens. In the first experiment, chickens were intracerebroventricular (ICV) injected with phosphate-buffered saline (PBS) and PNX-14 (0.8, 0.16, and 3.2 nmol). In second experiment, PBS, the antagonist of CRF/CRF receptors (astressin-B, 30 μg) and PNX-14 + astressin-B were injected. In the rest of the experiments chicken received astressin2-B (CRF receptor antagonist; 30 µg), SHU9119 (MCR/MCR receptor antagonist, 0.5nomol), MCL0020 (MCR receptor agonist, 0.5 nmol), B5063 (NPY receptor antagonist, 1.25 μg), SF22 (NPY receptor antagonist, 1.25 μg) and SML0891 (NPY receptor antagonist, 1.25 μg) rather than astressin-B. Then, cumulative intake of food was recorded for 2 h. Based on the findings, PNX-14 (0.16 and 3.2 nmol) led to increment in food consumption compared with the control (P < 0.05). Co-administration of the PNX-14 and astressin-B promoted PNX-14-induced hyperphagia (P < 0.05). Co-injection of the PNX-14 + astressin2-B potentiated hyperphagia PNX-14 (P < 0.05). Co-injection of PNX-14 + B5063 inhibited the effects of the PNX-14 (P < 0.05). The co-administration of the PNX-14 and SML0891 potentiated hypophagic effects of the PNX-14 (P < 0.05). The results showed that PNX-14-induced hyperphagia mediates via NPY, NPY and CRF/CRF receptors in neonatal chickens.
动物研究表明，神经肽 Y（NPY）、促肾上腺皮质激素和黑色素皮质素系统在奖励中具有中介作用，然而，这些物质如何与苯妥英-14（PNX-14）诱导的鸟类食物摄入相互作用仍有待确定。因此，本研究进行了八项实验，以研究 NPY、黑色素皮质素和促肾上腺皮质激素系统与新生鸡中 PNX-14 对食物消耗的潜在相互作用。在第一个实验中，鸡被脑室内（ICV）注射磷酸盐缓冲盐水（PBS）和 PNX-14（0.8、0.16 和 3.2nmol）。在第二个实验中，注射 PBS、CRF/CRF 受体拮抗剂（astressin-B，30μg）和 PNX-14+astressin-B。在其余的实验中，鸡接受了 astressin2-B（CRF 受体拮抗剂；30μg）、SHU9119（MCR/MCR 受体拮抗剂，0.5nomol）、MCL0020（MCR 受体激动剂，0.5nmol）、B5063（NPY 受体拮抗剂，1.25μg）、SF22（NPY 受体拮抗剂，1.25μg）和 SML0891（NPY 受体拮抗剂，1.25μg）而不是 stressin-B。然后，记录了 2 小时的累积食物摄入量。根据研究结果，与对照组相比，PNX-14（0.16 和 3.2nmol）导致食物摄入量增加（P<0.05）。PNX-14 与 astressin-B 共同给药促进了 PNX-14 诱导的多食症（P<0.05）。PNX-14+astressin2-B 的共同注射增强了 PNX-14 的多食症（P<0.05）。PNX-14+B5063 的共同注射抑制了 PNX-14 的作用（P<0.05）。PNX-14 与 SML0891 的共同给药增强了 PNX-14 的致厌食作用（P<0.05）。结果表明，PNX-14 诱导的多食症是通过新生鸡中的 NPY、NPY 和 CRF/CRF 受体介导的。
