BRAINSTEM MECHANISMS CONTROLLING JAW MOVEMENT

口面部运动行为的正常运作是必要的 人类的生存。哺乳动物的摄食行为始于 吮吸并发展到饮水和进食。目前， 很少有研究涉及大脑是如何组织产生这些 行为。甚至更少的是了解各种口腔运动的病因， 功能障碍如迟发性运动障碍。磨牙症和肌面疼痛 功能障碍综合征这项研究的长期目标是 了解中枢神经系统的机制 控制在活动期间发生的正常下颌运动，例如 进食和饮水，以及出现的异常下颌运动， 在各种疾病中。 这项建议的具体目的是继续调查， 细胞水平，进入控制下颌运动的神经元过程， 豚鼠我们将联合收割机技术与细胞内或全细胞膜片钳技术相结合 记录方法与逆行追踪技术，以确定 特定群体的下颌张开和关闭运动神经元，和三叉神经 薄脑切片和厚脑切片中的前运动神经元。该项目分为 两个主要部分。在第一部分中，我们将确定为确定下巴开瓶器， 更接近运动神经元和前运动神经元，I）存在特定的 神经细胞膜电导及其对神经元爆发作用 放电，2）这些电导是否是通过 两种单胺（5-HT和NE）。 第二部分将集中在兴奋性氨基酸介导的调节 通过单胺的突触传递。我们将确定是否有 5-羟色胺调节的基本相似性和差异， 突触的NMDA和非NMDA成分之间的去甲肾上腺素 V传入中脑向三叉神经运动神经元的传递 (Mes（五）。我们将通过记录化合物 Mes V核诱发的EPSP或EPSC和单纤维EPSP或EPSC 或单次Mes V神经元刺激。的结果 拟议的研究将提供深入了解细胞机制， 控制参与的不同神经元群体的放电 产生下颌运动，并将作为细胞基础， 神经元模型的咀嚼节律和爆发模式的产生。

The proper functioning of oral-facial motor behaviors is necessary for the survival of humans. The ingestive behaviors of mammals begins with suckling and progresses to drinking and feeding. Presently, there are very few studies addressing how the brain is organized to produce these behaviors. Even less is known about the etiology of various oral-motor dysfunctions such as tardive dyskinesia. bruxism, and myofacial pain dysfunction syndromes. The long-term goals of this research are to understand both the mechanism underlying the central nervous system control of normal jaw movements that occur during activities such as feeding and drinking, as well as the abnormal jaw movements that occur during various disorders. The specific aims of this proposal are to continue investigations, at the cellular level, into the neuronal processes controlling jaw movements in the guinea pig. We will combine intracellular or whole cell patch clamp recording methods with retrograde-tract tracing techniques to identify specific populations of jaw-opener and closer motoneurons, and trigeminal premotoneurons in thin and thick brain slices. The project is divided into two main parts. In part I, we will determine for identified jaw-opener and closer motoneurons and premotoneurons, I) the presence of specific intrinsic membrane conductances and their contribution to neuronal burst discharge, 2) whether these conductances are substrates for modulation by two monoamines (5-HT and NE). Part II will focus on modulation of excitatory amino acid mediated synaptic transmission by monoamines. We will determine if there are fundamental similarities and differences in modulation by serotonin and norepinephrine between NMDA and non-NMDA components of synaptic transmission to trigeminal motoneurons from mesencephalic of V afferents (Mes V). We will examine these relationships by recording the compound EPSP or EPSC and the single fiber EPSP or EPSC evoked from Mes V nucleus or single Mes V neuron stimulation, respectively. The results of the proposed studies will provide insights into the cellular mechanisms controlling discharge of distinct populations of neurons involved in production of jaw movements and will serve as a cellular foundation for neuronal models on masticatory rhythm and burst pattern generation.