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中枢 5-HT(2C)和 NMDA 受体在 LPS 诱导鸡摄食行为中的作用。

The role of central 5-HT(2C) and NMDA receptors on LPS-induced feeding behavior in chickens.

机构信息

Department of Physiology, Faculty of Veterinary Medicine, University of Tehran, 14155-6453, Tehran, Iran.

出版信息

J Physiol Sci. 2012 Sep;62(5):413-9. doi: 10.1007/s12576-012-0218-7. Epub 2012 Jun 27.

DOI:10.1007/s12576-012-0218-7
PMID:22735975
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10717554/
Abstract

In mammals, LPS regulate feeding primarily through the 5-HT(1A) and 5-HT(2c) receptors within the brain. However, the central effect of 5-HT(1A) and 5-HT(2c) on LPS-induced feeding behavior has not been studied in non-mammalian species. Also, the role of glutamatergic system in LPS-induced anorexia has never been examined in either mammalian or non-mammalian species. Therefore, in this study, we examined the role of serotonergic and glutamatergic systems on LPS-induced anorexia in chickens. Food intake was measured in chickens after centrally administered lipopolysaccharide (LPS) (20 ng) (0 h), followed by intracerebroventricular (ICV) injection of the 5-HT(1A) autoreceptor agonist (8-OH-DPAT, 61 nmol), 5-HT(2c) receptor antagonist (SB 242084, 30 nm), and NMDA receptor antagonist (DL-AP5, 5 nm) at the onset of anorexia (4 h). In the following experiments, we used DL-AP5 before 5-HT (10 μg) and SB242084 before glutamate (300 nm) for evaluation of the interaction between 5-HTergic and glutamatergic systems on food intake. The results of this study showed that SB 242084 and DL-AP5 significantly attenuated food intake reduction caused by LPS (P < 0.05) but 8-OH-DPAT had no effect. In addition, 5-HT-induced anorexia was significantly attenuated by DL-AP5 pretreatment (P < 0.05), while SB 242084 had no effect on glutamate-induced hypophagia. These results indicated that 5-HT and glutamate (via 5-HT(2c) and NMDA receptor, respectively) dependently regulate LPS-induced hypophagia in chickens.

摘要

在哺乳动物中,LPS 主要通过大脑中的 5-HT(1A)和 5-HT(2c)受体来调节摄食。然而,在非哺乳动物物种中,尚未研究中枢 5-HT(1A)和 5-HT(2c)对 LPS 诱导的摄食行为的影响。此外,无论是在哺乳动物还是非哺乳动物中,都从未研究过谷氨酸能系统在 LPS 诱导的厌食症中的作用。因此,在这项研究中,我们研究了 5-羟色胺能和谷氨酸能系统在鸡 LPS 诱导的厌食症中的作用。在 LPS(20ng)(0h)中枢给药后,测量鸡的食物摄入量,然后在厌食症发作时(4h)通过脑室内(ICV)注射 5-HT(1A)自身受体激动剂(8-OH-DPAT,61nmol)、5-HT(2c)受体拮抗剂(SB 242084,30nm)和 NMDA 受体拮抗剂(DL-AP5,5nm)。在后续实验中,我们在 5-HT(10μg)之前使用 DL-AP5 和在谷氨酸(300nm)之前使用 SB242084 来评估 5-羟色胺能和谷氨酸能系统对食物摄入的相互作用。这项研究的结果表明,SB 242084 和 DL-AP5 显著减弱了 LPS 引起的食物摄入减少(P<0.05),但 8-OH-DPAT 没有作用。此外,5-HT 引起的厌食症在 DL-AP5 预处理时明显减弱(P<0.05),而 SB 242084 对谷氨酸引起的食欲减退没有影响。这些结果表明,5-HT 和谷氨酸(分别通过 5-HT(2c)和 NMDA 受体)在鸡中独立调节 LPS 诱导的厌食症。

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