AXOPLASMIC TRANSPORT AND CENTRAL TRIGEMINAL PATTERN MAINTENANCE

颅面周围在大脑中的有序表征对于面部和头部的正常感觉和运动功能是必要的。虽然已经有相当多的实验关注中枢神经系统颅面表征的发育和可塑性，但我们仍然不明白它们是如何在整个生命中维持的。拟议研究的总体目标是了解维持啮齿动物三叉神经(V)系统中由外周决定的神经元细胞体和过程的中枢模式的必要条件。我们最近发现，长春碱对眶下神经（ION）轴突运输的衰减会导致所有中枢纤维相关模式的丧失。这是除离子横断外唯一被证明具有这种效果的产后操作，即使长春花碱处理的神经中的V初级传入神经元向外周和脑干的投射在质量上保持正常，也会发生这种情况。我们的工作假设是，V型脑干复合体中与触须相关的模式的保存需要两个条件：与触须相关的V神经节细胞的中央枝以与触须相对应的模式排列；在这个“模型”中，中央离子轴突的振动相关模式提供了相应的营养因子浓度梯度模式，这反过来又导致脑干神经元的持续聚集。V主核细胞的模式是丘脑和皮层中相应的触电相关模式的发展和维持所必需的。然而，任何一种神经营养物质都可能支持在切断或应用长春花碱治疗正在发育的离子后中枢V型模式的维持：1)这些操作导致继发于V神经节和脑干细胞死亡的中枢模式丧失。2)中枢模式丧失是由病变引起的发育中的脑干细胞功能输入异常引起的。2)中枢模式丧失是由病变引起的对发育中的V脑干复合体的功能输入异常引起的。3)特定肽（甘丙肽和神经肽Y0）在脑干复合体输入中的显著上调。Y)存活的V神经节细胞及其中央轴突在轴浆运输衰减或离子损伤后导致中央振动相关模式的丧失。本应用的实验将验证我们的工作假设，以及关于新生大鼠离子应用长春花碱后中央V模式丧失的机制的其他可能性。

Ordered representations of the craniofacial periphery in the brain are necessary for normal sensory and motor functions of the face and head. While considerable experimental attention has been paid to the development and plasticity of central nervous system craniofacial representations, we still do not understand how they are maintained throughout life. The overall aim of the proposed research is to understand the necessary conditions for maintenance of peripherally determined central patterns of neuronal cell bodies and processes in the rodent trigeminal (V) system. We recently showed that attenuation of axonal transport in the infraorbital nerve (ION) with vinblastine results in a loss of all central fibrissae-related patterns. This is the only postnatal manipulation other than ION transection that has ever been demonstrated to have this effect and it occurs even though V primary afferent neurons in vinblastine-treated nerve maintain qualitatively normal projections to the periphery and brainstem. Our working hypothesis is that two conditions are necessary for the preservation of vibrissae-related patterns in the V brainstem complex: arrangement of the central arbors of vibrissae-related V ganglion cells in a pattern corresponding to the vibrissae; and, delivery of a peripherally derived neurotrophic factor by these primary afferents to V brainstem neurons In this "model," the vibrissae-related patterning of central ION axons provides correspondingly patterned concentrations gradients of the trophic factor which, in turn, result in the maintained aggregation of brainstem neurons. The patterning of cells in V nucleus principalis is required for the development and maintenance of corresponding vibrissae-related patterns in thalamus and cortex. While any of several neurotrophins might support the maintenance of central V patterns following transection of, or application of vinblastine to, the developing ION: 1) These manipulations cause a loss of central patterns secondary to the death of V ganglion and brainstem cells. 2) Central pattern loss results from lesion-induced abnormal functional input to the developing brainstem cells. 2) Central pattern loss results from lesion-induced abnormal functional input to the developing V brainstem complex. 3) The dramatic up-regulation of specific peptides (galanin and neuropeptide Y0 in input to the developing brainstem complex. Y) in surviving V ganglion cells and their central axons contribute to the loss of central vibrissae-related patterns after attenuation of axoplasmic transport or damage to, the ION. The experiments in this application will test our working hypothesis as well as these other possibilities regarding the mechanisms underlying the loss of central V patterns after application of vinblastine to the ION in newborn rats.