据国外媒体报道，研究人员一项最新老鼠实验显示，大脑不依赖味觉机制便可以探测到食物中的卡路里。这种感知系统被称为“大脑第六感”，有利于科学家对人体肥胖的更深入理解。该研究发现暗示高糖易导致肥胖的玉米糖浆为什么受人们的喜爱并广泛地用于食物佐料。负责该研究的美国杜克大学研究人员伊凡·德·阿拉乔和同事们将该研究发表在3月27日出版的《神经元》杂志上。
在实验中，研究人员对老鼠基因进行了改变使其产生“盲糖”反应，使老鼠缺少能探测甜味食物的关键性味觉接受细胞。接下来研究人员将正常老鼠和盲糖老鼠分成两组观测它们饮用含糖液和无糖甜味溶液的具体反应，测试结果显示，盲糖老鼠不依赖于探测能力，在选择食物时更倾向于含高卡路里的糖液。
研究人员通过对盲糖老鼠大脑分析，表明大脑对食物的感应线路(reward circuitry)依赖于卡路里摄入量，独立于动物的味觉探测系统。分析结果显示大脑化学多巴胺含量作为感应线路的刺激中心随着卡路里摄入量增加而上升。同时，电生理学研究显示食物感应区域的神经元阿肯伯氏核(nucleus accumbens)受卡路里摄入量刺激，独立而味觉探测系统。
阿拉乔称，简要地进行概括，我们研究显示前侧多巴胺纹状体(dopamine-ventral striatum)感应系统，具有连接探测和分配美味食物的感应价值，可以在缺乏味觉接收信号情况下能够响应食物中的卡路里。因此，这些大脑路径并不排除对感观美食诱惑影响的编码，但也可能表现包括探测肠胃和新陈代谢信息的不确定性功能。
赞恩·安德鲁斯和托马斯·霍瓦斯在《神经元》杂志上发表评论称，这项大脑卡路里感应系统的发现，带给我们一些科学思考，比如：该研究对于人体肥胖发病机理和社会现象的重要理解和认识。(魏冬)
生物谷推荐原始出处：
Neuroscience Volume 120, Issue 4, 15 September 2003, Pages 1149-1156
Cholinergic interneurons of the nucleus accumbens and dorsal striatum are activated by the self-administration of cocaine
M. L. Berlangaa, C. M. Olsenb, V. Chenc, A. Ikegamib, B. E. Herringc, C. L. Duvauchellea, b, d and A. A. Alcantara, , a, c, d
a Institute for Neuroscience, The University of Texas at Austin, Austin, TX 78712, USA
b College of Pharmacy, The University of Texas at Austin, Austin, TX 78712, USA
c Department of Psychology, The University of Texas at Austin, Seay Building 4.212, Austin, TX 78712, USA
d The Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, Austin, TX 78712, USA
Accepted 25 April 2003. ; Available online 30 July 2003.
Abstract
The nucleus accumbens, a major component of the ventral striatum, and the dorsal striatum are primary targets of the mesolimbic dopamine pathway, which is a pathway that plays a critical role in reward and addiction. The shell compartment of the nucleus accumbens and the ventromedial striatum, in particular, receive extensive afferent projections from the ventral tegmental area, which is the major afferent source of the mesolimbic pathway [Prog Brain Res 99 (1993) 209; J Neurosci 7 (1987) 3915]. The present study focused on striatal cholinergic interneurons as potential key neurons involved in the neural basis of drug reinforcement. The main finding of this study is that cholinergic interneurons located in the shell compartment of the nucleus accumbens and the ventromedial striatum were activated, as measured by Fos labeling, following a 1 h session of the self-administration of cocaine in rats. A direct correlation existed between the percent of cholinergic interneurons that were activated and the amount of cocaine that was self-administered. The greatest amount of administered cocaine (approximately 10 mg/kg) resulted in the activation of approximately 80% of the cholinergic neurons. No such correlation existed in the group of animals that self-administered saline. In addition, activation was not found in the core compartment of the nucleus accumbens or the dorsolateral striatum, which receive extensive innervation from the substantia nigra and thus are more closely tied to the motor effects of the drug.
In conclusion, cocaine-driven neuronal activation was specific to the shell compartment of the nucleus accumbens (R2=0.9365) and the ventromedial striatum (R2=0.9059). These findings demonstrate that cholinergic interneurons are involved in the initial stage of cocaine intake and that these neurons are located in areas of the nucleus accumbens and dorsal striatum that are more closely tied to the rewarding and hedonic effects rather than the motor effects of cocaine intake.
