BRAINSTEM MECHANISMS CONTROLLING JAW MOVEMENT

口腔-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 哺乳，并发展到饮用和喂食。目前，有非常多的 很少有研究涉及大脑是如何组织产生这些的 行为。对于各种口腔运动的病因更是知之甚少 迟发性运动障碍等功能障碍。磨牙症和肌肉面部疼痛 功能障碍综合症。这项研究的长期目标是 了解中枢神经系统的潜在机制 控制在活动期间发生的正常下巴运动，例如 进食和饮水，以及发生的异常下巴运动 在各种疾病期间。 这项建议的具体目标是继续调查，在 在细胞水平上，进入控制颌骨运动的神经元过程 那只小白鼠。我们将结合细胞内或全细胞膜片钳 采用逆行追踪技术的记录方法以识别 令人瞠目结舌的运动神经元和更近的运动神经元以及三叉神经的特定种群 大脑薄片和厚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，我们将确定确定的令人瞠目结舌的 较近的运动神经元和前运动神经元，i)存在特定的 内在膜电导及其对神经元爆发的贡献 放电，2)这些电导是否为用于调制的衬底 两种单胺(5-羟色胺和去甲肾上腺素)。 第二部分将集中于兴奋性氨基酸介导的调制 单胺类突触传递。我们将确定是否有 5-羟色胺和5-羟色胺调节的基本异同 突触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 V)。我们将通过记录化合物来检查这些关系 EPSP或EPSC与MES V核单纤维诱发的EPSP或EPSC 或单个MES V神经元刺激。评选结果 拟议中的研究将提供对细胞机制的见解 控制不同群神经元的放电 产生下巴运动，并将作为细胞基础 咀嚼节律和爆裂模式产生的神经元模型。

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.