Taste and Visceral Integration in Parabrachial Nucleus

描述(申请人提供)：进食和代谢障碍，如 肥胖症、厌食症、暴食症、胃食道反流性恶病质、运动障碍和 嗅觉障碍会导致许多疾病，包括高血压、中风、 糖尿病和心脏病，因此在健康中占很大比例- 北美和其他国家的医疗费用。阐明神经 因此，控制进食的机制具有基本的临床意义。 意义。大量的行为研究表明，进食是由 味觉和内脏传入信号在中枢的整合 神经系统；然而，只有少数神经生理学研究 试图定位和描述这些机制。此应用程序将 评估味觉和内脏传入信号之间的神经相互作用 臂旁核(PBN)是一种脑干中继器，它能显著地接收 味觉和内脏传入的交叠。第一批实验将使用 标准的神经生理记录技术来检验这一假设 十二指肠营养和扩张信号以PBN表示，因为它们 没有在这个水平上描述，并且这些信号与胃相互作用 扩张反应。十二指肠信号与胃的相互作用 PBN的扩张和味觉反应将是神经生理学的 评估以检验这样一种假设，即伴随的饱足感在 PBN中味觉反应的内脏抑制形式。决赛 这一阶段的应用将进一步探讨PBN的内脏调节 通过尝试识别是否特定的品味反应 神经递质在调节这一效应方面发挥了作用。具体来说， 神经递质拮抗剂将被显微注射到离散的 在内脏和味觉刺激过程中记录的单个味觉细胞。 假设如果内脏对味觉反应的抑制 刺激是由所讨论的神经递质局部调节的，然后是拮抗 它的受体系统应该会逆转味觉抑制效应。识别 参与味觉内脏抑制的神经递质 PBN中的反应也可能提供关于其他中央机制的洞察 参与摄食控制的动物。

DESCRIPTION (provided by applicant): Feeding and metabolic disorders such as obesity, anorexia, bulimia, gastroesophageal reflux cachexia, dysgeusia, and anosmia contribute to numerous diseases including hypertension, stroke, diabetes, and heart disease, and thus account for a large proportion of health- care costs in North America and other countries. Elucidating the neural mechanisms that control feeding is, therefore, of fundamental clinical significance. Numerous behavioral studies indicate that feeding is regulated by the integration of taste and visceral afferent signals within the central nervous system; however, only a handful of neurophysiological studies have attempted to locate and characterize these mechanisms. This application will evaluate neural interactions between gustatory and visceral afferent signals in the parabrachial nucleus (PBN), a brainstem relay that receives significantly overlapping taste and visceral afferent inputs. The first experiments will use standard neurophysiological recording techniques to test the hypothesis that duodenal nutrient and distension signals are represented in PBN, as they have not been described at this level, and that these signals interact with gastric distension responses. The interaction of duodenal-signals with gastric distension and gustatory responses in PBN will then be neurophysiologically evaluated to test the hypothesis that a concomitant of satiation is expressed in the form of visceral suppression of palatable taste responses in PBN. The final phase of this application will further explore the visceral modulation of PBN taste responses through an attempt to identify whether particular neurotransmitters play a role in mediating the effect. Specifically, neurotransmitter antagonists will be microinjected into the discrete vicinity of single taste cells as they are recorded during visceral and taste stimulation. It is hypothesized that if the suppression of taste responses by visceral stimuli is mediated locally by the neurotransmitter in question, then antagonism of its receptor systems should reverse the taste suppression effect. Identifying the neurotransmitters that participate in the visceral suppression of taste responses in PBN may also provide insight regarding other central mechanisms that participate in feeding control.