Brain Center Rudolf Magnus, Department of Translational Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.
Department of Animals in Science and Society, Division of Behavioural Neuroscience, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands.
Sci Rep. 2019 Jan 31;9(1):1050. doi: 10.1038/s41598-018-37405-w.
The homeostatic need for sodium is one of the strongest motivational drives known in animals. Although the brain regions involved in the sensory detection of sodium levels have been mapped relatively well, data about the neural basis of the motivational properties of salt appetite, including a role for midbrain dopamine cells, have been inconclusive. Here, we employed a combination of fiber photometry, behavioral pharmacology and c-Fos immunohistochemistry to study the involvement of the mesocorticolimbic dopamine system in salt appetite in rats. We observed that sodium deficiency affected the responses of dopaminergic midbrain neurons to salt tasting, suggesting that these neurons encode appetitive properties of sodium. We further observed a significant reduction in the consumption of salt after pharmacological inactivation of the nucleus accumbens (but not the medial prefrontal cortex), and microstructure analysis of licking behavior suggested that this was due to decreased motivation for, but not appreciation of salt. However, this was not dependent on dopaminergic neurotransmission in that area, as infusion of a dopamine receptor antagonist into the nucleus accumbens did not alter salt appetite. We conclude that the nucleus accumbens, but not medial prefrontal cortex, is important for the behavioral expression of salt appetite by mediating its motivational component, but that the switch in salt appreciation after sodium depletion, although detected by midbrain dopamine neurons, must arise from other areas.
体内钠稳态平衡的需求是动物中已知的最强烈的动机驱动因素之一。尽管已经相对较好地绘制出了参与感知钠水平的大脑区域图谱，但关于盐欲的动机特性的神经基础的数据，包括中脑多巴胺细胞的作用，仍然没有定论。在这里，我们采用光纤光度测定法、行为药理学和 c-Fos 免疫组织化学相结合的方法，研究了中脑边缘多巴胺系统在大鼠盐欲中的作用。我们观察到，钠缺乏会影响多巴胺能中脑神经元对盐味觉的反应，这表明这些神经元编码了钠的食欲特性。我们进一步观察到，在化学损毁伏隔核（但不是内侧前额叶皮质）后，盐的消耗量显著减少，舔行为的微观结构分析表明，这是由于对盐的动机降低，而不是对盐的欣赏减少所致。然而，这并不依赖于该区域的多巴胺能神经传递，因为向伏隔核内注射多巴胺受体拮抗剂不会改变盐欲。我们的结论是，伏隔核而不是内侧前额叶皮质，对于通过调节其动机成分来表达盐欲的行为很重要，但在钠耗竭后对盐的欣赏的转变，尽管被中脑多巴胺神经元检测到，但必须来自其他区域。
