NEUROPHYSIOLOGICAL STUDIES OF VOMITING

恶心和呕吐（呕吐）通常与癌症有关 化疗和放疗，术后恢复，运动和空间 疾病、怀孕和各种疾病，包括艾滋病。长期 这个项目的目标是确定产生的神经机制， 在各种情况下呕吐。增加对神经系统的了解 涉及的电路，以及对神经递质的不断增长的知识 受体亚型，应导致改善药物 对策将使用“虚构呕吐”进行研究 实验模型，其特点是一系列的突发性的 共同激活的运动神经（膈）和腹部运动神经， 去大脑瘫痪的猫具体目标是调查 触发或抑制呕吐的神经输入和中枢神经元 产生呕吐的电路，包括涉及的前运动神经元 在产生呼吸肌激活的模式中， 呕吐的动作。 胃迷走神经、肝迷走神经和内脏神经输入对 将确定是否引发呕吐，以及可能的相互作用 迷走神经和内脏神经输入之间的关系以及该区域的重要性 postrema介导迷走神经诱发的呕吐。初步研究 表明孤束髓核（NTS）可能发挥作用， 一个重要的作用，作为一个整合网站，为不同的催吐输入。NTS 神经元将被测试以确定它们是否接收到会聚兴奋 从不同的输入能够引发呕吐，包括该地区 后化学感受器呕吐触发区和腹部迷走神经， 前庭神经，以及对各种催吐药物， 作为癌症化疗剂顺铂。呕吐引起的 大范围的输入可以被大脑中未知的传入所抑制。 颈迷走神经这种抑制性输入的来源是 确定，因为它的止吐作用的可能性是 通过抑制由会聚兴奋的NTS神经元介导 催吐输入。 腹部和肋间内呼气运动神经元接受中枢神经系统的刺激， 呼吸驱动来自球脊髓前运动呼气神经元， 尾腹呼吸组（VRG）。呕吐期间，尾部 VRG呼气神经元以两种不同的模式放电， 适合于驱动腹部和内部肋间运动神经元， 在呕吐的时候会彼此异相发射细胞内 尾侧VRG呼气神经元的记录将确定 相位抑制产生了这两种放电模式。在 此外，还将搜索可能提供VRG神经元的神经元。 膈神经兴奋性驱动源和共同活动源仍然未知 呕吐时肋间运动神经元的变化。最后，研究将 对控制上气道的贡献， 呕吐的神经元投射在背疑核（在 尾侧VRG）至含有运动神经元的疑核 支配上呼吸道肌肉组织。

Nausea and vomiting (emesis) commonly occur in association with cancer chemo- and radiation therapy, post-operative recovery, motion and space sickness, pregnancy, and various diseases including AIDS. The long-term goal of this project is to determine the neural mechanisms that produce vomiting under various conditions. Increased understanding of the neural circuitry involved, together with a growing knowledge of neurotransmitter receptor subtypes, should lead to improved pharmaceutical countermeasures. Studies will be conducted using the "fictive vomiting" experimental model, which is characterized by a series of bursts of coactivation of diaphragmatic (phrenic) and abdominal motor nerves in decerebrate, paralyzed cats. The specific objectives are to investigate neural inputs that trigger or inhibit vomiting and the central neuronal circuitry that produces vomiting, including pre-motor neurons involved in generating the pattern of respiratory muscle activation critical for the motor act of vomiting. The potential for gastric vagal, hepatic vagal, and splanchnic inputs to trigger vomiting will be determined, as will possible interactions between vagal and splanchnic inputs and the importance of the area postrema in mediating vagal-induced vomiting. Preliminary studies indicate that the medullary nucleus of the solitary tract (NTS) may play an important role as an integrating site for different emetic inputs. NTS neurons will be tested to determine if they receive convergent excitation from different inputs capable of triggering vomiting, including the area postrema chemoreceptor emetic trigger zone and abdominal vagus and vestibular nerves, as well as in response to various emetic drugs such as the cancer chemotherapeutic agent cisplatin. Vomiting elicited by a broad range of inputs can be inhibited by unknown afferents in the cervical vagus nerve. The source of this inhibitory input will be determined, as will the possibility that its anti-emetic effects are mediated by inhibition of NTS neurons that are excited by convergent emetic inputs. Abdominal and internal intercostal expiratory motoneurons receive central respiratory drive from bulbospinal pre-motor expiratory neurons located in the caudal ventral respiratory group (VRG). During vomiting, caudal VRG expiratory neurons fire in two distinct patterns, which are appropriate to drive abdominal and internal intercostal motoneurons that fire out of phase with each other during vomiting. Intracellular recordings from caudal VRG expiratory neurons will determine the role of phasic inhibitory puts in producing these two discharge patterns. In addition, a search will be conducted for VRG neurons that may provide the still unknown source of excitatory drive to phrenic and co-active external intercostal motoneurons during vomiting. Finally, a study will be made of the contribution to the control of the upper airway during vomiting by a projection from neurons in the nucleus retroambigualis (in the caudal VRG) to the nucleus ambiguous, which contains motoneurons innervating upper airway musculature.