Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell
Daily bingeing on sugar repeatedly releases dopamine in the accumbens shell
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DOI：
10.1016/j.neuroscience.2005.04.043
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发表时间：
2005-01-01
期刊：
影响因子：
3.3
通讯作者：
Hoebel, BG
中科院分区：
文献类型：
--
作者：
Rada, P;Avena, NM;Hoebel, BG
大多数药物滥用增加多巴胺（DA）在脑桥核（NAc），并这样做每次作为一种药理学反应。可口的食物也会释放贝壳DA，但在幼稚的大鼠中，这种效果会在长时间进食时减弱，并随着重复而消失。在特定的饮食环境下，糖可能会产生类似于滥用药物的影响。当给予间歇性接触蔗糖时，大鼠表现出DA致敏和阿片依赖的迹象，如DA和μ阿片受体的改变，与苯丙胺和酒精的交叉致敏，以及纳洛酮促戒断的行为和神经化学迹象。目前的实验是为了研究依赖蔗糖的大鼠是否在每次暴饮暴食时都会释放DA。我们还预测，乙酰胆碱（ACh），这上升作为一顿饭结束时，将被延迟在大鼠间歇性获得蔗糖。为了产生依赖性，实验组（每日间断蔗糖）维持12小时食物剥夺的饮食，延长4小时至黑暗，然后12小时获得10%蔗糖溶液和食物，每天，持续21天。作为主要的结果，这些大鼠逐渐增加他们的蔗糖摄入量从37至112毫升每天（从13至20毫升，在第一个小时的访问），并反复增加细胞外DA的130%的基线，在第一天，第2天和第21天的蔗糖访问的第一个小时期间，通过微透析在NAc壳中测量。三个对照组在第21天未能显示出细胞外DA的显著增加：在第1天和第21天仅蔗糖1小时（蔗糖两次），随意获得蔗糖和食物（每日随意蔗糖），以及间歇性食物代替蔗糖（每日间歇性食物）。在所有组中，与DA同时测量的乙酰胆碱在接近结束时和每次试验餐后显著增加。在每日间断蔗糖组中，最高ACh水平（133%）发生在蔗糖餐结束后的第一次采样期间。总之，蔗糖依赖的动物有一个延迟的乙酰胆碱饱足反应，喝更多的蔗糖，并释放更多的DA比蔗糖或暴饮暴食的经验，但非依赖的动物。这些结果表明，间歇性暴饮蔗糖和滥用药物之间的另一个神经化学相似性：两者都可以反复增加NAc壳中的细胞外DA。(c)2005年IBRO。由爱思唯尔有限公司出版。保留所有权利。
Most drugs of abuse increase dopamine (DA) in the nucleus accumbens (NAc), and do so every time as a pharmacological response. Palatable food also releases accumbens-shell DA, but in naive rats the effect can wane during a long meal and disappears with repetition. Under select dietary circumstances, sugar can have effects similar to a drug of abuse. Rats show signs of DA sensitization and opioid dependence when given intermittent access to sucrose, such as alterations in DA and mu-opioid receptors, cross-sensitization with amphetamine and alcohol, and behavioral and neurochemical signs of naloxone-precipitated withdrawal. The present experiment asks whether sucrose-dependent rats release DA each time they binge. We also predict that acetylcholine (ACh), which rises as the end of a meal, will be delayed in rats with intermittent access to sucrose. To create dependency, the experimental group (Daily Intermittent Sucrose) was maintained on a diet of 12-h food deprivation that extended 4 h into the dark, followed by 12-h access to a 10% sucrose solution and chow, daily, for 21 days. As the main result, these rats gradually increased their sucrose intake from 37 to 112 ml per day (from 13 to 20 ml in the first hour of access), and repeatedly increased extracellular DA to 130% of baseline as measured in the NAc shell by microdialysis during the first hour of sucrose access on day 1, day 2 and day 21. Three control groups failed to show a significant increase in extracellular DA on day 21: Sucrose only for 1 h on days 1 and 21 (Sucrose Twice), ad libitum access to sucrose and chow (Daily Ad libitum Sucrose), and intermittent chow instead of sucrose (Daily Intermittent Chow). Acetylcholine measured at the same time as DA, increased significantly toward the end and after each test meal in all groups. In the Daily Intermittent Sucrose group, the highest ACh levels (133%) occurred during the first sample after the sucrose meal ended. In summary, sucrose-dependent animals have a delayed ACh satiation response, drink more sucrose, and release more DA than sucrose- or binge-experienced, but non-dependent animals. These results suggest another neurochemical similarity between intermittent bingeing on sucrose and drugs of abuse: both can repeatedly increase extracellular DA in the NAc shell. (c) 2005 IBRO. Published by Elsevier Ltd. All rights reserved.