Department of Basic Sciences, Faculty of Veterinary Medicine, University of Tehran, 14155-6453 Tehran, Iran.
Department of Basic Sciences, Faculty of Veterinary Medicine, University of Tehran, 14155-6453 Tehran, Iran.
Neurosci Lett. 2024 Jan 1;818:137557. doi: 10.1016/j.neulet.2023.137557. Epub 2023 Nov 14.
The study was performed to evaluate the role of central serotoninergic, GABAergic, and cholecystokinin systems in neuropeptide VF (NPVF)-induced hypophagia in broiler chickens. In this study, 9 experiments were designed, each with one control and three treatment groups (n = 44 in each experiment). Control chicks of all groups were subjected to normal saline + Evans blue 0.1 % Intracerebroventricular (ICV) injection. In the first experiment, 3 groups of chicks received NPVF (4, 8, and 16 nmol). In experiment 2-9, one group of chicks received NPVF (16 nmol), another received 10 µg fluoxetine (serotonin reuptake inhibitor) (experiment 2), 1.25 µg PCPA (serotonin synthesis inhibitor) (experiment 3), 1.5 µg SB-242,084 (5-HT receptor antagonist) (experiment 4), 15.25 nmol 8-OH-DPAT (5-HT receptor antagonist) (experiment 5), 0.5 µg picrotoxin (GABA receptor antagonist) (experiment 6), 20 ng CGP54626 (GABA receptor antagonist) (experiment 7), 1 nmol devazepide (CCK receptor antagonist) (experiment 8), and 1 nmol/L(-|-),260 (CCK receptor antagonist) (experiment 9), and another final group received combination of specific neurotransmitter + NPVF Then, the cumulative food intake was measured until 120 min post-injection. ICV injection of NPVF (8 and 16 nmol) significantly decreased food intake (P < 0.05). Simultaneous injection of fluoxetine + NPVF and also picrotoxin + NPVF significantly increased hypophagia caused by NPVF (P < 0.05). However, co-administration of PCPA + NPVF and also SB242084 + NPVF significantly decreased NPVF-induced hypophagia (P < 0.05). Finally, 8-OH-DPAT, CGP54626, devazepide, and L-365,260 had no effect on the hypophagia brought on by NPVF (P > 0.05). Count-type behaviors were dose-dependent and decreased in groups that received NPVF compared to the control group (P < 0.05). Our finding recommended an interconnection between central NPVF and serotoninergic, GABAergic, and cholecystokinin systems in neonatal chickens.
本研究旨在评估中枢 5-羟色胺能、γ-氨基丁酸能和胆囊收缩素系统在肉鸡神经肽 VF（NPVF）诱导的摄食减少中的作用。本研究共设计了 9 项实验，每个实验均有一个对照组和三个处理组（每组 44 只）。所有组别的对照鸡均接受生理盐水+Evans 蓝 0.1%脑室内（ICV）注射。在第一项实验中，三组鸡接受 NPVF（4、8 和 16nmol）。在实验 2-9 中，一组鸡接受 NPVF（16nmol），另一组接受 10µg 氟西汀（5-羟色胺再摄取抑制剂）（实验 2）、1.25µg PCPA（5-羟色胺合成抑制剂）（实验 3）、1.5µg SB-242,084（5-羟色胺受体拮抗剂）（实验 4）、15.25nmol 8-OH-DPAT（5-羟色胺受体拮抗剂）（实验 5）、0.5µg 印防己毒素（GABA 受体拮抗剂）（实验 6）、20ng CGP54626（GABA 受体拮抗剂）（实验 7）、1nmol devazepide（CCK 受体拮抗剂）（实验 8）和 1nmol/L（-|-），260（CCK 受体拮抗剂）（实验 9），另一组鸡则接受特定神经递质+NPVF 的联合注射。然后，测量注射后 120 分钟内的累积食物摄入量。NPVF（8 和 16nmol）的 ICV 注射显著降低了食物摄入量（P<0.05）。氟西汀+NPVF 以及印防己毒素+NPVF 的同时注射显著增加了 NPVF 引起的摄食减少（P<0.05）。然而，PCPA+NPVF 和 SB242084+NPVF 的联合给药显著降低了 NPVF 引起的摄食减少（P<0.05）。最后，8-OH-DPAT、CGP54626、devazepide 和 L-365,260 对 NPVF 引起的摄食减少没有影响（P>0.05）。计数型行为呈剂量依赖性，与对照组相比，接受 NPVF 的组减少（P<0.05）。我们的研究结果表明，新生鸡的中枢 NPVF 与 5-羟色胺能、γ-氨基丁酸能和胆囊收缩素系统之间存在相互联系。
