Characterization of 3D feeding kinematics and EMG of rats and laminar specific single cell encoding properties in the motor cortex

大鼠 3D 进食运动学和肌电图的表征以及运动皮层层状特定单细胞编码特性

• 批准号: 10006877
• 负责人: Kazutaka Takahashi
• 金额: $ 16.2万
• 依托单位: UNIVERSITY OF CHICAGO
• 依托单位国家: 美国
• 财政年份: 2019
• 资助国家: 美国
• 起止时间: 2019-09-04 至 2022-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10006877
• 关键词: 3-Dimensional; Aging; Animal Model; Aspiration Pneumonia; Behavior; Behavioral; Biomechanics; Bolus Infusion; Brain Stem; Brain region; Bruxism; Cells; Central Nervous System Diseases; Choking; Chronic; Clinical; Complex; Data; Deglutition; Deglutition Disorders; Dental; Dental Implants; Development; Dimensions; Disease; Dysarthria; Effectiveness; Electrodes; Exhibits; Feeding behaviors; Food; Future; Generations; Genetic Techniques; Goals; Health; Impairment; Implant; Ingestion; Injury; Jaw; Knowledge; Lead; Life; Limb structure; Liquid substance; Literature; Longitudinal Studies; Malnutrition; Mammals; Mastication; Measurement; Microelectrodes; Missouri; Modeling; Motor; Motor Cortex; Movement; Muscle; Neuronal Plasticity; Neurons; Oral; Output; Pathologic; Patients; Peripheral; Pharmacology; Play; Prevention; Process; Property; Quality of life; Rattus; Reflex action; Regulation; Rehabilitation therapy; Research; Roentgen Rays; Role; Sensorimotor functions; Site; Speed; Structure; Techniques; Temporomandibular Joint Disorders; Testing; Tongue; Tooth Loss; Video Recording; Work; awake; base; behavior change; central nervous system injury; chronic painful condition; craniofacial; craniofacial structure; disability; dynamic system; environmental change; experimental study; feeding; improved; innovation; insight; kinematics; malignant tongue neoplasm; motor control; motor impairment; nervous system disorder; neurological rehabilitation; neuromechanism; neurophysiology; novel; oral motor; orofacial; pleasure; prevent; relating to nervous system; soft tissue; treatment effect; vocal cord

Project summary Impaired chewing, swallowing as a result of orofacial or CNS injury or disease is a worldwide health problem that can impact quality of life and even be life-threatening. Current rehabilitation of such impairments has largely overlooked recent advances in neurorehabilitation of limb motor control which may explain why many patients cannot regain normal chewing and swallowing. The oral primary motor cortex (oM1) is the main brain region involved in the generation and control of orofacial movements. However, detailed baseline 3D kinematics and EMGs of aerodigestive and craniofacial structure as a whole which is to be compared to the pathological cases is lacking. Detailed characterization of modulations of local field potentials (LFPs) to gape types remains unclear. Furthermore, detailed kinematic and EMG encoding in single unit spiking activities for any orofacial behavior has not been performed. Lastly, relation between LFPs and muscle activities has not been explored except for beta oscillation and tongue muscles. Thus, to fill in the gap in our knowledge, our specific aims are: AIM 1: To characterize and quantify 3D kinematics of aerodigestive and craniofacial structures and jaw and tongue electromyographic (EMG) activities during natural feeding in awake rats. We will utilize our documented expertise with 3D high-speed videofluoroscopy and chronically implanted jaw/tongue EMG electrodes. We will: (a) characterize gape cycle types (e.g., chewing, swallowing) during feeding and how epiglottal and vocal fold open/closure are timed at each of the cycle types; and (b) perform dimension reduction techniques on both kinematics and EMGs to obtain a set of principal movements and EMG activities for each cycle type and transitions between cycle type. AIM 2: To relate the jaw/tongue EMG and 3D kinematics of aerodigestive and craniofacial structures to simultaneously record neural activities within multiple oM1 sites and layers in awake rats, and test if and how oM1 neural activity properties are related to tongue and jaw EMG and 3D kinematics of aerodigestive and craniofacial structures during feeding. We will utilize our documented expertise with chronically implanted microelectrode arrays that span horizontally and vertically into oM1 layers 2/3 (mainly cortico-cortico projections) and 5/6 (mainly output projections). We will then: (a) characterize how LFP profiles are related to types of gape cycles and their transitions between them; (b) characterize how kinematic- and EMG activities are encoded in single unit spiking activity of oM1; and (c) characterize cortico-muscular coherence between oM1 LFPs and jaw/tongue EMG activities for each gape type. This proposal will define a new 3D kinematic characterization of aerodigestive and craniofacial structures during feeding and novel oM1 neural mechanisms in terms of modulations of LFPs to gape cycles and single unit spiking activity encoding of kinematics and EMG based on layers. Better understanding of such mechanisms is needed to develop improved prevention and management of impaired motor functions resulting from oral injury, possibly by targeting oM1 neural processes.

项目总结 口腔面部或中枢神经系统损伤或疾病导致的咀嚼、吞咽障碍是一个世界性的健康问题。 这可能会影响生活质量，甚至危及生命。目前对这种损伤的康复已经 在很大程度上忽视了肢体运动控制神经康复的最新进展，这可能解释了为什么许多 患者无法恢复正常的咀嚼和吞咽。口腔初级运动皮质(OM1)是大脑的主要部分 参与口腔面部运动的产生和控制的区域。然而，详细的基线3D 空气、消化和颅面整体结构的运动学和肌电图，并与 缺乏病理病例。局域场势(LFP)对GaP调制的详细表征 类型尚不清楚。此外，在单个单位尖峰活动中详细的运动学和肌电编码 还没有进行过任何口腔面部行为。最后，LFP和肌肉活动之间的关系还没有 除了贝塔振荡和舌肌外，其他都被研究过了。因此，为了填补我们知识的空白，我们的 具体目标是：目标1：描述和量化空气消化和颅面部的三维运动学 清醒状态下自然进食时的结构和颌舌肌电活动 老鼠。我们将利用我们记录在案的3D高速视频透视和长期植入的专业知识 颌部/舌部肌电电极。我们将：(A)确定张口周期的类型(例如，咀嚼、吞咽) 喂养以及会厌和声带在每种周期类型下的打开/关闭时间；以及(B)执行 运动学和肌电的降维技术，以获得一组主要动作和 每种周期类型的肌电活动以及周期类型之间的转换。目的2：将颌骨/舌头肌电联系起来 以及空气消化和颅面结构的3D运动学，以同时记录神经 清醒大鼠多个OM1部位和层内的活动，并测试OM1神经活动是否和如何 舌颌肌电信号和空气、消化、颅面三维运动学特征相关 在进食过程中的结构。我们将利用我们记录在案的专业知识进行长期植入的微电极 水平和垂直跨越到OM1层2/3(主要是皮质-皮质投影)和5/6的阵列 (主要是产出预测)。然后，我们将：(A)描述LFP曲线与GAPE周期类型之间的关系 以及它们之间的转换；(B)表征运动学和肌电活动如何以单一的 OM1的单位尖峰活动；以及(C)表征OM1 LFP和OM1 LFP之间的皮质-肌肉一致性 每种张口类型的下颌/舌头肌电活动。该提案将定义一种新的3D运动学特征 进食过程中的空气消化和颅面结构以及新的OM1神经机制 LFP对张口周期的调制及运动学和肌电的单单位峰活动编码 层次感。需要更好地了解这种机制，以改进预防和管理 口腔损伤导致的运动功能受损，可能是通过靶向OM1神经突起。