DENTAL AND OROFACIAL PAIN BRAIN STEM MECHANISMS

我们的研究计划的长期目标是澄清中央 急性和慢性牙齿和口面疼痛的潜在机制及其 控制 我们最近的NIH支持的研究导致了重大的新进展， 深入了解三叉神经（V）脑干复合体的神经可塑性， 并进入深层脑干机制（例如肌肉;以及 颞下颌关节，TMJ）以及皮肤（面部）疼痛。 的 我们记录的神经可塑性在Adhesivbracelem中的表达 牙髓的牙髓内神经传导阻滞揭示了复杂性。 在 脊髓躯体感觉系统，外周神经传入障碍也可以诱导 躯体感觉通路的改变被视为一种反射 的神经可塑性和作为神经系统的发展作出贡献， 慢性疼痛。 机制作为促进发展的工具 慢性疼痛。 这些变化背后的机制，在抑制 现有的传入输入。 我们对V型braviem细胞的研究表明， 动物上颌骨或下颌牙髓的去传入 机械感受场的统计学显著变化， 在口腔神经元中特别明显的反应特性;这些 使用更广泛的纸浆，效果显著延长 麻木。 然而，对于脊柱系统， 我们记录的生理变化背后的传入神经阻滞后， 果肉不清晰。 因此，我们将测试假设，下颌 牙髓传入神经阻滞与（A）上颌骨出芽有关 口核V亚核正常归属区的传入 下颌区的代表;（B）传入神经减少 抑制;和（C）初级传入去极化（PAD）减少 这被认为是突触前抑制的反映。 比较 正常和去传入成年动物之间的这些特征 在V脑干神经元或初级传入的定量分析 对于B & C假设，利用我们在以下方面的丰富专业知识： 细胞外单个单元记录。 解决假设A，新 我们实验室的方法涉及V神经分支的HRP标记， 细胞内HRP标记生理学鉴定的单个单位将 被使用。 这些研究将阐明一些可能的机制， 参与脑损伤后V-脑干复合体的神经可塑性反应 牙髓可能是慢性口面 痛苦

The long-term objectives of our research program are to clarify the central mechanisms underlying acute and chronic dental and orofacial pain and its control. Our recent NIH-supported research has resulted in major new insights into the neuroplasticity of the trigeminal (V) brainstem complex, and into brainstem mechanisms underlying deep (e.g. muscle; and temporomandibular joint, TMJ) as well as cutaneous (facial) pain. THE EXPRESSION OF NEUROPLASTICITY THAT WE DOCUMENTED IN THE ADULT v BRAINSTEM COMPLEX WAS REVEALED BY ENDODONTIC DEAFFERENTATION OF THE TOOTH PULP. IN THE SPINAL SOMATOSENSORY SYSTEM, PERIPHERAL DEAFFERENTATION CAN ALSO INDUCE ALTERATIONS IN SOMATOSENSORY PATHWAYS THAT HAVE BEEN VIEWED AS A REFLECTION OF CNS NEUROPLASTICITY AND AS PROCESSES CONTRIBUTING TO THE DEVELOPMENT OF CHRONIC PAIN. THE MECHANISMS AS PROCESSES CONTRIBUTING TO THE DEVELOPMENT OF CHRONIC PAIN. THE MECHANISMS UNDERLYING THESE CHANGES IN INHIBITION OF EXISTING AFFERENT INPUTS. OUR STUDIES OF V BRAINSTEM CELLS INDICATED THAT MAXILLARY OR MANDIBULAR PULP DEAFFERENTATION IN ADULT ANIMALS RESULTED IN STATISTICALLY SIGNIFICANT ALTERATIONS IN MECHANORECEPTIVE FIELD AND RESPONSE PROPERTIES THAT WERE ESPECIALLY APPARENT IN ORALS NEURONS; THESE EFFECTS WERE SIGNIFICANTLY PROLONGED WITH MORE EXTENSIVE PULP DEAFFERENTATION. AS FOR THE SPINAL SYSTEM, HOWEVER, the mechanisms underlying our documented physiological changes after deafferentation of the pulp are unclear. THEREFORE, we will test hypotheses that mandibular pulp deafferentation is associated with (A) SPROUTING OF MAXILLARY AFFERENTS INTO REGIONS OF V SUBNUCLEUS ORALIS NORMALLY DEVOTED TO THE REPRESENTATION OF THE MANDIBULAR DIVISION; (B) a decrease in afferent inhibition; and (C) a decrease in primary afferent depolarization (PAD) WHICH IS CONSIDERED A REFLECTION OF PRESYNAPTIC INHIBITION. Comparison of these features between normal and deafferented adult animals will be made in V brainstem neurons or primary afferents IN QUANTITATIVE ANALYSES UTILIZING, FOR HYPOTHESES B & C, OUR WELL-DOCUMENTED EXPERTISE IN EXTRACELLULAR SINGLE UNIT RECORDING. TO ADDRESS HYPOTHESIS A, NEW APPROACHES FOR OUR LAB INVOLVING HRP LABELLING OF V NERVE BRANCHES AND INTRACELLULAR HRP LABELLING OF PHYSIOLOGICALLY IDENTIFIED SINGLE UNITS WILL BE USED. THESE STUDIES WILL CLARIFY SOME OF THE MECHANISMS THAT MAY BE INVOLVED IN NEUROPLASTIC RESPONSES OF THE V BRAINSTEM COMPLEX TO INJURY OF THE TOOTH PULP AND THAT MAY UNDERLIE THE DEVELOPMENT OF CHRONIC OROFACIAL PAIN.