Anandamide improves food intake and orexinergic neuronal activity in the chronic sleep deprivation induction model in rats by modulating the expression of the CB1 receptor in the lateral hypothalamus

IF 2.5 3区医学 Q3 ENDOCRINOLOGY & METABOLISM

Neuropeptides Pub Date : 2023-10-01 DOI:10.1016/j.npep.2023.102336

Rafie Belali , Seyyed Ali Mard , Seyed Esmaeil Khoshnam , Kowsar Bavarsad , Alireza Sarkaki , Yaghoob Farbood

{"title":"Anandamide improves food intake and orexinergic neuronal activity in the chronic sleep deprivation induction model in rats by modulating the expression of the CB1 receptor in the lateral hypothalamus","authors":"Rafie Belali , Seyyed Ali Mard , Seyed Esmaeil Khoshnam , Kowsar Bavarsad , Alireza Sarkaki , Yaghoob Farbood","doi":"10.1016/j.npep.2023.102336","DOIUrl":null,"url":null,"abstract":"<div>Sleep deprivation alters orexinergic neuronal activity in the lateral hypothalamus (LH), which is the main regulator of sleep-wake, arousal, appetite, and energy regulation processes. Cannabinoid receptor (CBR) expression in this area is involved in modulating the function of orexin neurons. In this study, we investigated the effects of endocannabinoid anandamide (AEA) administration on improving food intake and appetite by modulating the activity of orexin neurons and CB1R expression after chronic sleep deprivation. Adult male Wistar rats (200–250 g) were randomly divided into three groups: control + vehicle (Control), chronic sleep deprivation + vehicle (SD), and chronic sleep deprivation +20 mg/kg AEA (SD + A). For SD induction, the rats were kept in a sleep deprivation device for 18 h (7 a.m. to 1 a.m.) daily for 21 days. Weight gain, food intake, the electrical power of orexin neurons, CB1R mRNA expression in hypothalamus, CB1R protein expression in the LH, TNF-α, IL-6, IL-4 levels and antioxidant activity in hypothalamus were measured after SD induction. Our results showed that AEA administration significantly improved food intake (p < 0.01), Electrical activity of orexin neurons (p < 0.05), CB1R expression in the hypothalamus (p < 0.05), and IL-4 levels (p < 0.05). AEA also reduced mRNA expression of OX1R and OX2R (p < 0.01 and p < 0.05 respectively), also IL-6 and TNF-α (p < 0.01) and MDA level (p < 0.05) in hypothalamic tissue. As a consequence, AEA modulates orexinergic system function and improves food intake by regulating the expression of the CB1 receptor in the LH in sleep deprived rats.</div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"101 ","pages":"Article 102336"},"PeriodicalIF":2.5000,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuropeptides","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0143417923000173","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}

引用次数: 0

Abstract

Sleep deprivation alters orexinergic neuronal activity in the lateral hypothalamus (LH), which is the main regulator of sleep-wake, arousal, appetite, and energy regulation processes. Cannabinoid receptor (CBR) expression in this area is involved in modulating the function of orexin neurons. In this study, we investigated the effects of endocannabinoid anandamide (AEA) administration on improving food intake and appetite by modulating the activity of orexin neurons and CB1R expression after chronic sleep deprivation. Adult male Wistar rats (200–250 g) were randomly divided into three groups: control + vehicle (Control), chronic sleep deprivation + vehicle (SD), and chronic sleep deprivation +20 mg/kg AEA (SD + A). For SD induction, the rats were kept in a sleep deprivation device for 18 h (7 a.m. to 1 a.m.) daily for 21 days. Weight gain, food intake, the electrical power of orexin neurons, CB1R mRNA expression in hypothalamus, CB1R protein expression in the LH, TNF-α, IL-6, IL-4 levels and antioxidant activity in hypothalamus were measured after SD induction. Our results showed that AEA administration significantly improved food intake (p < 0.01), Electrical activity of orexin neurons (p < 0.05), CB1R expression in the hypothalamus (p < 0.05), and IL-4 levels (p < 0.05). AEA also reduced mRNA expression of OX1R and OX2R (p < 0.01 and p < 0.05 respectively), also IL-6 and TNF-α (p < 0.01) and MDA level (p < 0.05) in hypothalamic tissue. As a consequence, AEA modulates orexinergic system function and improves food intake by regulating the expression of the CB1 receptor in the LH in sleep deprived rats.

查看原文本刊更多论文

Anandamide通过调节下丘脑外侧CB1受体的表达，改善大鼠慢性睡眠剥夺诱导模型中的食物摄入和食欲能神经元活性

睡眠剥夺改变了下丘脑外侧（LH）的食欲能神经元活动，LH是睡眠觉醒、唤醒、食欲和能量调节过程的主要调节器。大麻素受体（CBR）在该区域的表达参与调节食欲素神经元的功能。在这项研究中，我们研究了内源性大麻素anandamide（AEA）在慢性睡眠剥夺后通过调节食欲素神经元的活性和CB1R的表达来改善食物摄入和食欲的作用。成年雄性Wistar大鼠（200-250 g）随机分为三组：对照组+赋形剂（对照组）、慢性睡眠剥夺+赋形器（SD）和慢性睡眠剥夺+20 mg/kg AEA（SD+A）。对于SD诱导，将大鼠在睡眠剥夺装置中保持18小时（上午7点至凌晨1点），持续21天。SD诱导后，测定体重增加、食物摄入、食欲素神经元的电能、下丘脑CB1R mRNA的表达、LH CB1R蛋白的表达、TNF-α、IL-6、IL-4水平以及下丘脑抗氧化活性。我们的研究结果表明，AEA给药显著改善了食物摄入（p＜0.01）、食欲素神经元的电活性（p＜0.05）、下丘脑CB1R的表达（p＞0.05）和IL-4水平（p＜05）。AEA还降低了OX1R和OX2R的mRNA表达（分别为p＜0.01和p＜0.05，下丘脑组织中IL-6和TNF-α（p＜0.01）以及MDA水平（p＜0.05）。因此，AEA通过调节睡眠剥夺大鼠LH中CB1受体的表达来调节食欲系统功能并改善食物摄入。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Neuropeptides 医学-内分泌学与代谢

CiteScore

5.40

自引率

6.90%

发文量

审稿时长

>12 weeks

期刊介绍： The aim of Neuropeptides is the rapid publication of original research and review articles, dealing with the structure, distribution, actions and functions of peptides in the central and peripheral nervous systems. The explosion of research activity in this field has led to the identification of numerous naturally occurring endogenous peptides which act as neurotransmitters, neuromodulators, or trophic factors, to mediate nervous system functions. Increasing numbers of non-peptide ligands of neuropeptide receptors have been developed, which act as agonists or antagonists in peptidergic systems. The journal provides a unique opportunity of integrating the many disciplines involved in all neuropeptide research. The journal publishes articles on all aspects of the neuropeptide field, with particular emphasis on gene regulation of peptide expression, peptide receptor subtypes, transgenic and knockout mice with mutations in genes for neuropeptides and peptide receptors, neuroanatomy, physiology, behaviour, neurotrophic factors, preclinical drug evaluation, clinical studies, and clinical trials.