Taste and Visceral Integration in Parabrachial Nucleus

描述（由申请人提供）：进食和代谢障碍，如 肥胖症、厌食症、贪食症、胃食管反流性恶病质、味觉障碍和 嗅觉丧失导致许多疾病，包括高血压，中风， 糖尿病和心脏病，因此占健康的很大比例- 北美和其他国家的医疗费用。阐明神经 因此，控制进食的机制是基本的临床 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内的整合 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）是一个脑干中继， 重叠的味觉和内脏传入输入。第一个实验将使用 标准的神经生理学记录技术来测试假设， 十二指肠营养和扩张信号在PBN中表示，因为它们具有 在这个水平上没有被描述过，这些信号与胃 膨胀反应胃电信号与胃电活动的相互作用 然后，PBN中的膨胀和味觉反应将被神经生理学地 评估以检验这一假设，即饱食的伴随表现在 PBN中适口性味觉反应的内脏抑制形式。最终 本申请的第一阶段将进一步探索PBN的内脏调节 通过尝试识别特定的 神经递质在介导该效应中起作用。具体地说， 神经递质拮抗剂将被显微注射到离散的附近， 单个味觉细胞，因为它们在内脏和味觉刺激期间被记录。 据推测，如果抑制味觉反应的内脏 刺激是由所讨论的神经递质局部介导的，然后是拮抗作用。 它的受体系统应该可以逆转味觉抑制效应。识别 参与味觉内脏抑制的神经递质 PBN的反应也可以提供关于其他中枢机制的见解 参与控制进食的细胞

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.