PONTINE GUSTATORY RESPONSES FOLLOWING SODIUM DEFICIENCY

本研究探讨了一种激发状态，即钠食欲，对桥脑臂旁核（PBN）味觉神经反应的影响。这些核处理味觉和内脏感觉信息，涉及盐的食欲和各种其他摄食行为和调节系统。双侧PBN损伤阻止大鼠表达钠的食欲。在盐和至少3种其他标准化学物质（蔗糖、柠檬酸和盐酸奎宁）的浓度范围下，在钠补充或缺乏的大鼠中，评估单个PBN味觉神经元的细胞外记录。最初，钠的食欲会通过饮食剥夺而增加。随后的研究将使用标准的利尿剂方案，速尿，来诱导快速钠缺乏。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、正常的动物中执行。这些平行的研究对于我自己的训练（急性记录比慢性记录更容易）来说是可取的，而且因为已经有证据表明来自孤立束核的外周和第一中枢味觉神经元对盐的食欲的影响。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与动机行为发展相关的潜在神经机制，盐的食欲。

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.