英国《每日邮报》网站7月12日报道题：为什么盐会上瘾：它就像香烟和麻醉品一样刺激脑细胞。

研究人员说，盐会像香烟和麻醉品一样让人上瘾，对盐的渴求会刺激同样的基因、脑细胞和大脑连接神经元。

这一发现将有助于解释，为什么许多人明明知道盐会影响血压和心脏健康，却仍然难以控制盐的摄入量。

在研究中，澳大利亚和美国的科学家给一组实验鼠提供低盐食物，另一组则进行盐水滴注。

他们将这些老鼠的脑部活动与正常饮食的老鼠的脑部活动进行了比较。他们还让一些老鼠3天不摄入盐，然后再让它们尽情喝盐水，在此过程中观察它们的脑部活动。

当老鼠需要盐时，脑细胞就会产生与海洛因、可卡因和尼古丁等上瘾物质有关的蛋白质。

墨尔本大学教授德里克·登顿说：“在这项研究中，我们发现，对盐的本能需求会产生促使对鸦片和可卡因上瘾的神经结构。”研究还显示，摄入盐之后，大脑在盐还没有真正进入血液系统并流经大脑之前就已感到满足。

研究人员说，盐对整体健康的重要性意味着，人对盐的需求是深深植根在大脑中的“古老本能”。这也能解释为什么我们对咸味食物如此偏爱。

试验还显示，阻止老鼠从吃盐中获得快感能在一定程度上减少它对盐的需求。研究报告发表在《国家科学院院刊》（PNAS）上。

原文出处：

Proceedings of the National Academy of Sciences     DOI： 10.1073/pnas.1109199108

Relation of addiction genes to hypothalamic gene changes subserving genesis and gratification of a classic instinct, sodium appetite

Liedtke, Wolfgang B.; McKinley, Michael J.; Walker, Lesley L.; Zhang, Hao; Pfenning, Andreas R.; Drago, John; Hochendoner, Sarah J.; Hilton, Donald L.; Lawrence, Andrew J.; Denton, Derek A.

Sodium appetite is an instinct that involves avid specific intention. It is elicited by sodium deficiency, stress-evoked adrenocorticotropichormone (ACTH), and reproduction. Genome-wide microarrays in sodium-deficient mice or after ACTH infusion showed up-regulationof hypothalamic genes, including dopamine- and cAMP-regulated neuronal phosphoprotein 32 kDa (DARPP-32), dopamine receptors-1and -2, α-2C- adrenoceptor, and striatally enriched protein tyrosine phosphatase (STEP). Both DARPP-32 and neural plasticityregulator activity-regulated cytoskeleton associated protein (ARC) were up-regulated in lateral hypothalamic orexinergic neuronsby sodium deficiency. Administration of dopamine D1 (SCH23390) and D2 receptor (raclopride) antagonists reduced gratificationof sodium appetite triggered by sodium deficiency. SCH23390 was specific, having no effect on osmotic-induced water drinking,whereas raclopride also reduced water intake. D1 receptor KO mice had normal sodium appetite, indicating compensatory regulation.Appetite was insensitive to SCH23390, confirming the absence of off-target effects. Bilateral microinjection of SCH23390 (100nM in 200 nL) into rats’ lateral hypothalamus greatly reduced sodium appetite. Gene set enrichment analysis in hypothalamiof mice with sodium appetite showed significant enrichment of gene sets previously linked to addiction (opiates and cocaine).This finding of concerted gene regulation was attenuated on gratification with perplexingly rapid kinetics of only 10 min,anteceding significant absorption of salt from the gut. Salt appetite and hedonic liking of salt taste have evolved over >100million y (e.g., being present in Metatheria). Drugs causing pleasure and addiction are comparatively recent and likely reflectusurping of evolutionary ancient systems with high survival value by the gratification of contemporary hedonic indulgences.Our findings outline a molecular logic for instinctive behavior encoded by the brain with possible important translational–medicalimplications.