PONTINE GUSTATORY RESPONSES FOLLOWING SODIUM DEFICIENCY

这项研究调查了一种动机状态，即食欲，对桥臂旁核(PBN)的味觉神经反应的影响。这些核团处理味觉和内脏感觉信息，涉及食盐和其他各种摄食行为和调节系统。双侧损毁PBN会阻止大鼠表现出钠的食欲。在钠充足或缺乏的大鼠的SAID刺激过程中，将评估单个PBN味觉神经元的细胞外记录，刺激范围为氯化钠和至少3种其他标准化学物质，蔗糖、柠檬酸和奎宁。最初，钠的食欲将通过饮食剥夺来提高。随后的研究将使用一种标准的利尿剂方案速尿，以引起快速的钠缺乏。至少饮食方案将在急性准备、轻度麻醉的大鼠和长期准备、清醒、行为正常的动物中执行。这些平行研究对于我自己的训练都是可取的(急性记录比慢性记录更容易)，也因为已经有证据表明，孤束核中外周和第一个中央味觉神经元的食盐偏好会产生影响。除了一个例外，所有这些先前的研究都是在麻醉的大鼠身上进行的。来自这些实验的数据将提供对潜在的神经机制的洞察，这些神经机制与动机行为的发展有关，即食盐。

The research in this proposal investigates the influence that a motivated state, sodium appetite, has on gustatory neural responses in the pontine parabrachial nuclei (PBN). These nuclei process gustatory and visceral sensory information involved in salt appetite and a variety of other ingestive behaviors and regulatory systems. Bilateral damage to the PBN prevents a rat from expressing a sodium appetite. Extracellular recordings from single PBN gustatory neurons will be assessed during sapid stimulation with a concentration range of NaCl and at least 3 other standard chemicals, sucrose, citric acid and quinine HCl in rats that are either sodium replete or deficient. Initially, the sodium appetite will be raised by dietary deprivation. Subsequent studies will use a standard diuretic regimen, furosemide, to induce a rapid sodium deficiency. At least the dietary protocol will be performed in both acutely prepared, lightly anesthetized rats and chronically prepared, awake, behaving animals. These parallel studies are desirable both for my own training (acute recording is easier than chronic) and because evidence already exists on the effects of salt appetite from peripheral and the first central gustatory neurons in the nucleus of the solitary tract. With one exception, all these prior studies were in anesthetized rats. The data from these experiments will provide insight into the potential neural mechanisms related to development of a motivated behavior, salt appetite.