MOTOR/SENSORY SPECIFICITY--MECHANISMS AND AUGMENTATION

手术修复受损的周围神经往往不能 恢复足够的功能。再生轴突的误区是 这是这次失败的主要原因。运动轴突触达皮肤 没有提供功能，堵塞了它们占据的道路； 到达肌肉的皮肤轴突可能会起作用，但会提供 信息不正确。最近的实验表明， 这个问题的解决方案。大鼠运动神经轴突的再生 股神经产生多条侧支发芽；运动/感觉 通过修剪皮肤侧支来提高特异性 神经，同时保持那些在肌肉神经。专一性可能是 在修复前通过挤压神经来增加增强 侧枝萌发形成和路径取样。如果一个类似的 在神经缝合时可产生效果，结果 临床神经修复的可能性可以大大提高。这个 拟议的实验旨在进一步表征 通过侧枝修剪产生特异性的过程，以及 找出扩增它的技术，这可能是 应用于临床神经修复。Aim I更清楚地定义了 神经挤压增加特异性的机制，并寻求 将增加的特异性与改善的功能联系起来。目标 II寻求刺激运动的再生侧枝萌发 轴突和后续再生的特异性应用 营养因子以受控的方式直接作用于修复部位。 这些操作产生的函数将是 与再生专一性相关。这些实验开始了 指导临床应用特异度的方法 增强功能。AIM III利用了更大的专一性 对青少年进行观察，以进一步了解这种机制 运动/感觉特异性，并介绍了一种新的神经移植物 用幼年轴突和虎皮整合成体通路的模型 反之亦然，以确定随年龄而恶化的成分。这个 幼年和老年大鼠侧枝萌发的程度将是 与最终再生专一性相关。目标四证据 对皮神经的运动轴突支进行修剪 是通过轴突追踪技术获得的。这些实验 将寻求形态和电生理方面的确认 修剪。Aim V扩展了我们对特定运动的观察 比较运动神经和感觉神经AS的通路特征 移植物用于再生运动轴突。初步实验 表明运动神经实际上是优越的，这一发现如果 确诊将具有直接、直接的临床意义。

Surgical repair of injured peripheral nerve often fails to restore adequate function. Misdriction of regenerating axons is a primary cause of this failure. Motor axons reaching skin provide no function and block the pathways which they occupy; cutaneous axons reaching muscle may function, but will provide incorrect information. Recent experiments suggest a possible solution to this problem. Motor axons regenerating in the rat femoral nerve produce multiple collaterals sprouts; motor/sensory specificity is improved by pruning collaterals from cutaneous nerve while keeping those in muscle nerve. Specificity may be enhanced by crushing the nerve before repair to increase collateral sprout formation and pathway sampling. If a similar effect could be produced at the time of nerve suture, the outcome of clinical nerve repair could be substantially improved. The proposed experiments are designed to further characterize the process of specificity generation through collateral pruning, and to identify techniques for its amplification which could be applied to clinical nerve repair. Aim I more clearly defines the mechanism by which nerve crush increases specificity, and seeks to correlate increased specificity with improved function. Aim II seeks to stimulate regenerative collateral sprouting of motor axons and subsequent regeneration specificityby application of trophic factors directly the repair site in a controlled manner. The function resulting from these manipulations will be correlated with regeneration specificity. These experiments open the way to direct clinical application of specificity enhancement. Aim III takes advantage of the greater specificity observed in juveniles to gain further insights into the mechanism of motor/sensory specificity, and introduces a novel nerve graft model which confornts adult pathways with juvenile axons and vice versa, to identify components which deteriorate with age. The extent of collateral sprouting in juvenile and aged rats will be correlated with final regeneration specificity. Aim IV Evidence for pruning of motor axon collaterals from cutaneous nerve has been obtained with axon tracing techniques. These experiments will seek morphologic and electrophysiologic confirmation of pruning. Aim V extends our observations of specific motor pathway characteristics to compare motor and sensory nerve as graft for regenerating motor axons. Preliminary experiments suggest that motor nerve is in fact superior, a finding which if confirmed will have immediate, direct clinical relevance.