BRAIN STEM MECHANISMS CONTROLLING JAW MOVEMENT

这项建议的具体目的是进一步描绘神经元的 控制有节奏的下颌运动（RJM）的机制类似于 豚鼠的咀嚼我们将联合收割机， 神经解剖学和神经药理学技术来定义 脑干回路及其潜在机制 由咀嚼肌的刺激引起的有节奏的下颌运动 皮层我们建议：1）确定特定神经信使的作用 在短脉冲时控制三叉神经前运动神经元兴奋性 训练皮层刺激或在重复皮层刺激诱导的RJM期间 刺激. 2)确定已识别三叉神经的位置 前运动神经元，含有谷氨酸、血清素或去甲肾上腺素， 3)确定哪些三叉神经前运动神经元亚群 咀嚼皮质中产生的离皮质传入的特定靶点。 该项目分为两个主要部分。在第一部分，单细胞 记录和微离子电渗喷射技术将被用来 确定特定神经信使在控制中的重要性 皮层诱导的RJM期间三叉神经前运动神经元兴奋性。 在皮质诱导的RJM期间记录识别的前运动神经元 同时应用假定的神经信使激动剂， 对手。第二部分将集中在利用神经解剖学和 免疫组织化学技术，以进一步表征的作用， 三叉神经前运动神经元在RJM产生中的作用的第一集合中 实验中，我们将联合收割机免疫组化技术， 逆行示踪技术鉴定神经递质 三叉神经前膜神经元亚群的定位 前运动神经元含有下列神经信使：谷氨酸， 血清素和去甲肾上腺素在第二组实验中， 将进行标记实验以确定 三叉神经前运动神经元特异性接受离皮层神经元输入 咀嚼皮层的组织 这项研究的长期目标是了解这两种机制 中枢神经系统对正常节律性下颌的控制 在进食和饮水等活动中发生的运动， 也不正常不自主的，发生在紊乱中的下颌运动 如迟发性运动障碍、磨牙症和肌筋膜疼痛功能障碍 综合征产生这些异常颌运动的病因 是未知的，尽管磨牙症被认为与压力有关， 迟发性运动障碍到基底神经元多巴胺活性的破坏 神经节在豚鼠中进行的拟议实验的结果将 提供了对神经生理学和药理学的见解 机制，以及脑干水平的解剖基质， 下意识的有节奏的下颌运动， 人类

The specific aims of this proposal are to further delineate the neuronal mechanisms controlling rhythmical jaw movements (RJMs) resembling mastication in the guinea pig. We will combine electrophysiological, neuroanatomical, and neuropharmacological techniques to define the brainstem circuits and their underlying mechanisms responsible for rhythmical jaw movements induced by stimulation of the masticatory cortex. We propose to 1) determine the role of specific neuromessengers in controlling trigeminal premotoneuronal excitability during short pulse train cortical stimulation or during RJMs induced by repetitive cortical stimulation. 2) establish the location(s) of identified trigeminal premotoneurons which contain glutamate, serotonin, or norepinephrine, and 3) determine which subpopulation of trigeminal premotoneurons are specific targets of corticofugal afferents arising in masticatory cortex. The project is divided into two main parts. In part I, single cell recording and microiontophoretic ejection techniques will be utilized to determine the importance of specific neuromessengers in the control trigeminal premotoneuronal excitability during cortically induced RJMs. Identified premotoneurons will be recorded during cortically induced RJMs while simultaneously applying putative neuromessenger agonists and antagonists. Part II will focus on utilizing neuroanatomical and immunohistochemical techniques to further characterize the roles of trigeminal premotoneurons in RJM production. In the first set of experiments, we will combine immunohistochemical techniques for neurotransmitter identification with retrograde tracer techniques for trigeminal premontoneuronal localization of subpopulations of premotoneurons which contain the following neuromessengers: glutamate, serotonin, and norepinephrine. In the second series of experiments double labelling experiments will be performed to determine the subpopulation of trigeminal premotoneurons which specifically receive corticofugal input from masticatory cortex. The long-term goal of this research is to understand both the mechanism underlying the central nervous system control of normal rhythmic jaw movements that occur during activities such as feeding and drinking, as well as the abnormal. Involuntary, jaw movements occurring in disorders such as tardive dyskinesia, bruxism and myofascial pain dysfunction syndrome. The etiology of the generation of these abnormal jaw movements is unknown, although bruxism is thought to be related to stress, and tardive dyskinesia to a disruption of dopamine activity in the basal ganglia. The results of the proposed experiments in the guinea pig will provide insights into the neurophysiological and pharmacological mechanisms, as well as anatomical substrates at the brainstem level, underlying the production of involuntary rhythmic jaw movements in humans.