NEUROPHYSIOLOGICAL STUDIES OF VOMITING

长期目标是确定 产生呕吐，这是一个潜在的严重问题，通常 运动和放射病，癌症患者的治疗， 和获得性免疫缺陷综合征(AIDS)。初步研究 将调查主要呼吸肌的控制情况 (腹部和横隔膜)产生压力变化 对呕吐负责，长期目标是 确定呕吐时这个神经回路是如何被激活的 在不同的条件下产生。 我们将从各种单一的脑干神经元中记录 “假想呕吐”在去大脑、瘫痪的猫身上 研究不同细胞群在对照中的可能作用 呕吐时这些呼吸肌的变化。虚构的呕吐是 由一种共同激活的特征模式所定义 腹肌神经，对催吐剂的反应， 这预计会在未瘫痪的动物身上产生呕吐。 将要研究的细胞包括下行吸气神经元。 背侧和腹侧延髓呼吸组(DRG、VRG) 在上颈髓(CL-C2)，向尾侧突出 头端VRG的Botzinger复合体中的呼气神经元，以及 中缝隐核(产生膈神经)内的神经元 兴奋)和背侧网状结构(已经 其他人建议包含一个“呕吐中心”)。 腹肌已被证明保持活跃 去除呼气神经元兴奋性输入后的呕吐 在尾侧视网膜节。脊髓反射的可能作用 呕吐过程中的腹肌激活将在 通过比较切割后的腹部活动来去掉猫的大脑 选定的脊背根(消除脊髓传入输入 或在T1-2脊髓切开后(消除下行输入)。 切断尾侧VRG呼气神经元轴突的作用 对腹神经活动的影响也将在虚构的 呕吐(即，在脊柱伸展反射的制剂中 不会被引出)。 还将进行一系列损伤实验，以更好地 勾画出正常生活所必需的脑干区域 (虚构的)期间主要呼吸肌的活动 呕吐。 更好地理解产生呕吐的途径应该 导致更有效的药物对策。

The long-term goal is to determine the neural mechanisms that produce vomiting, a potentially serious problem commonly associated with motion and radiation sickness, treatment of cancer patients, and acquired immune deficiency syndrome (AIDS). Initial studies will investigate the control of the major respiratory muscles (abdominal and diaphragm) that produce the pressure changes responsible for vomiting, with the longer term objective of determining how this neural circuitry is engaged when vomiting is produced during various conditions. We will record from a variety of single brain stem neurons during "fictive vomiting" in decerebrate, paralyzed cats in order to investigate the possible role of various cell groups in the control of these respiratory muscles during vomiting. Fictive vomiting is defined by a characteristic pattern of co-activation of phrenic and abdominal muscle nerves, elicited in response to emetic agents, that would be expected to produce vomiting in unparalyzed animals. Cells that will be studied include descending inspiratory neurons in the dorsal and ventral medullary respiratory groups (DRG, VRG) and in the upper cervical spinal cord (Cl-C2), caudally projecting expiratory neurons in the Botzinger complex of the rostral VRG, and neurons in the raphe obscurus nucleus (which produce phrenic nerve excitation) and dorsal-lateral reticular formation (which has been suggested by others to contain a "vomiting center"). The abdominal muscles have been shown to remain active during vomiting after removal of excitatory input from expiratory neurons in the caudal VRG. The possible contribution of spinal reflexes to abdominal muscle activation during vomiting will be examined in decerebrate cats by comparing abdominal activity after cutting selected spinal dorsal roots (eliminating spinal afferent inputs or after spinal section at T1-2 (eliminating descending inputs). The effects of cutting the axons of caudal VRG expiratory neurons on abdominal nerve activity will also be determined during fictive vomiting (i.e., in a preparation in which spinal stretch reflexes would not be elicited). A series of lesion experiments will also be carried out to better delineate the brain stem regions that are necessary for normal activation of the major respiratory muscles during (fictive) vomiting. Better understanding of the pathways that produce vomiting should lead to more effective pharmaceutical countermeasures.