课题基金 / 基金详情

DENTAL AND OROFACIAL PAIN--BRAIN STEM MECHANISMS

DENTAL AND OROFACIAL PAIN--BRAIN STEM MECHANISMS
牙齿和口面部疼痛——脑干机制
批准号:
2129001
负责人:
BARRY J. SESSLE
金额:
$16.09万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
1978
资助国家:
美国
项目状态:
已结题
起止时间:
1978-01-01 至 1996-05-31

项目摘要

项目成果

BARRY J. SESSLE的其他基金

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中文摘要
翻译
我们的长期目标是阐明中央机制和 神经母细胞是急性和慢性疼痛的潜在原因。而C-的变化- 纤维功能被认为与几种慢性疼痛有关, C-纤维传入在神经元正常发育中的作用 中枢躯体感觉通路的特性,更不用说 发展成紊乱的疼痛行为,目前仍不清楚。C-纤维的作用 向V脑干和脊髓提供伤害性传入兴奋性传入 和脊髓神经元,但最近的研究引起了人们对 C纤维也可能对神经效应和神经营养产生影响 努力;这些神经母细胞的影响包括塑造神经元感受性 伤害性和非伤害性的场和反应特性 小路。C纤维在糖尿病的正常发育过程中有类似的作用吗? 这些特性属于V型体感系统吗?我们将解决这一问题 问题,通过检验:假设I,新生儿C- 纤维传入引起感受野和反应的改变 成人V亚核尾侧亚核伤害性神经元的特性 脑干复合体;假设II,新生儿C纤维耗竭 传入产生感受野和反应的改变 下丘脑低阈值机械感受性神经元的特性 成年V脑干复合体的尾侧亚核;和假设III, 新生儿C-纤维传入的耗竭会导致 低阈值的感受野和反应特性 成人主要感觉核团的机械感受性神经元 V脑干复合体。因为C纤维初级传入不投射到 新生儿辣椒素与V主感觉核的变化 给药是对尾神经调节作用的一种改变 对主要感觉神经元的作用;因此,我们还将测试:假设 四、新生儿C-纤维传入耗竭引起的改变 在尾侧亚核对感受器的调制影响中 低阈值机械感受器的场和响应特性 成体V脑干复合体主要感觉核内的神经元。 对于每一系列实验,新生大鼠都将被注射 辣椒素耗尽C-纤维传入,然后在2-3月龄 我们将描述这些特性,并与对照动物进行比较 V亚核尾侧亚核中神经元的数量 脑干传递伤害性信息,或在主要感觉中 在触觉中起主要LTM脑干继电器作用的核 通向大脑皮层的路径。在两组动物中,主要感觉神经元 属性也将在操作升序过程中进行测试 局麻药或谷氨酸对尾侧神经的调节作用 尾部注射。这些研究的意义在于它们 与V脑干内神经母细胞突起的完整联系 复合体及其感受场和反应特性的决定因素 V型躯体感觉神经元以及改变C纤维功能的观点 可能参与了几种慢性疼痛状况的发展。
英文摘要
Our long-term objectives is to elucidate the central mechanisms and neuroblastic underlying acute and chronic pain. While alterations in C- fiber function have been implicated in several chronic pain conditions, the role of C-fiber afferent in the normal development of neuronal properties in central somatosensory pathways, let alone in the development of disordered pain behavior, is still unclear. C-fibers do provide nociceptive afferent excitatory inputs to V brainstem and spinal and spinal neurons, but recent studies have drawn attention to the possible neuroeffector and neurotrophic influences that C fibers may also exert; these neuroblastic influence including shaping neuronal receptive field and response properties in both nociceptive and non-nociceptive pathways. Do C-fibers have a similar role in the normal development of these properties i the V somatosensory system? We will address this question, by testing: Hypothesis I, that the neonatal depletion of C- fiber afferent produces alterations in the receptive field and response properties of nociceptive neurons in subnucleus caudalis of the adult V brainstem complex; Hypothesis II, that the neonatal depletion of C-fiber afferent produces alterations in the receptive field and response properties of low-threshold mechanoreceptive (LTM) neurons in the subnucleus caudalis of the adult V brainstem complex; and Hypothesis III, that the neonatal depletion of C-fiber afferent produces alterations in the receptive field and response properties of low-threshold mechanoreceptive (LTM) neurons in the main sensory nucleus of the adult V brainstem complex. Since C-fiber primary afferent do not project to the V main sensory nucleus changes associated with neonatal capsaicin administration is an alteration to the modulatory influence that caudalis exerts on main sensory neurons; we will therefore also test: Hypothesis IV, that the neonatal depletion of C-fiber afferent produces alteration in the modulatory influences of subnucleus caudalis on the receptive field and response properties of low-threshold mechanoreceptive (LTM) neurons in the main sensory nucleus of the adult V brainstem complex. For each series of experiments, neonatal rats will be injected with capsaicin to deplete their C-fiber afferent and then at 2-3 months of age we will characterize, and compare with control animals, the properties of neurons in V subnucleus caudalis, which acts as the as the primary brainstem relay of nociceptive information, or in the main sensory nucleus which acts as the principal LTM brainstem relay in the vibrissa pathway to cortex. In both groups of animals, main sensory neuronal properties will also be tested during manipulation of the ascending caudalis modulatory influences by local anesthetic or glutamate injections of caudalis. The significance of these studies lies in their integral link to neuroblastic processes operating in the V brainstem complex and the determinants of receptive field and response properties of V somatosensory neurons, and to the view that altered C-fiber function may be involved in the development of several chronic pain conditions.
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PERIPHERAL NMDA RECEPTORS AND TMD PAIN MECHANISMS
  • 批准号:
    6897831
  • 项目类别:
  • 资助金额:
    $30.67万
  • 财政年份:
    2003
  • 负责人:
    BARRY J. SESSLE
  • 依托单位:
PERIPHERAL NMDA RECEPTORS AND TMD PAIN MECHANISMS
  • 批准号:
    6687476
  • 项目类别:
  • 资助金额:
    $27.0万
  • 财政年份:
    2003
  • 负责人:
    BARRY J. SESSLE
  • 依托单位:
PERIPHERAL NMDA RECEPTORS AND TMD PAIN MECHANISMS
  • 批准号:
    6904853
  • 项目类别:
  • 资助金额:
    $5.27万
  • 财政年份:
    2003
  • 负责人:
    BARRY J. SESSLE
  • 依托单位:
PERIPHERAL NMDA RECEPTORS AND TMD PAIN MECHANISMS
  • 批准号:
    6795580
  • 项目类别:
  • 资助金额:
    $27.0万
  • 财政年份:
    2003
  • 负责人:
    BARRY J. SESSLE
  • 依托单位: