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Lack of evidence for a role of serotonin in interleukin-1-induced hypophagia.

机译:缺乏证据表明5-羟色胺在白介素1引起的吞咽障碍中的作用。

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Interleukin-1 (IL-1) administration depresses food intake in rodents. IL-1 is known to increase the metabolism of serotonin, which is known to affect feeding behavior. Thus, serotonin is an obvious candidate for a mediator of the hypophagic response to IL-1. Therefore, we tested the ability of serotonergic agonists and antagonists to alter the hypophagic responses to IL-1 and bacterial lipopolysaccharide (LPS). Hypophagia was assessed in ad lib-fed mice by recording the intake of sweetened milk in a 30-min period. Acute intraperitoneal administration of mouse IL-1beta reliably decreased milk intake. This hypophagic response was not affected by any of the serotonin antagonists tested, including 5-HT(1A) (WAY100135 and propranolol), 5-HT(1B) (GR127935), 5-HT(2) (ritanserin, ketanserin, SB206553, and RS102221), mixed 5-HT(1/2) (methysergide and metergoline), and 5-HT(3) (tropisetron) receptor antagonists. The 5-HT(1A) agonists (8-OH-DPAT and ipsapirone) and a 5-HT(1B) agonist (CGS12066B) known to decrease the activity of serotonergic neurons, also had no effect. Mice pretreated with 5,7-dihydroxytryptamine to deplete brain serotonin ate less, but, nevertheless, displayed similar hypophagic responses to mIL-1beta or LPS. The results suggest that serotonin is not involved in the decrease in short-term milk intake induced by mIL-1beta or LPS in mice that have been fed ad lib.
机译:白介素-1(IL-1)的给药会降低啮齿动物的食物摄入量。已知IL-1会增加血清素的代谢,这会影响进食行为。因此,5-羟色胺显然是介导对IL-1的吞噬反应的候选者。因此,我们测试了血清素能激动剂和拮抗剂改变对IL-1和细菌脂多糖(LPS)的低相反应的能力。通过记录30分钟内甜牛奶的摄入量来评估自由喂养小鼠的吞咽能力。小鼠IL-1beta的急性腹膜内给药可靠地减少了牛奶的摄入。这种低吞噬反应不受任何5-HT(1A)(WAY100135和普萘洛尔),5-HT(1B)(GR127935),5-HT(2)(ritanserin,ketanserin,SB206553,和RS102221),混合的5-HT(1/2)(甲基麦角酰麦角龙和美特古琳)和5-HT(3)(托吡司琼)受体拮抗剂。 5-HT(1A)激动剂(8-OH-DPAT和ipsapirone)和5-HT(1B)激动剂(CGS12066B)已知会降低血清素能神经元的活性,但也没有作用。用5,7-二羟基色胺预处理以减少脑5-羟色胺的小鼠吃得少,但是对mIL-1beta或LPS表现出相似的低吞噬反应。结果表明,5-羟色胺不参与随意喂养的小鼠中由mIL-1beta或LPS诱导的短期牛奶摄入量的减少。

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