What is the mechanism for paresthesia following nerve injury?

1.免疫组织化学研究：神经损伤后三叉神经尾侧核内P物质分布的时空变化(1)新生辣椒素治疗可导致成人三叉神经尾侧核深层P物质消失，2周龄时恢复的三叉神经尾侧核浅层P物质一过性减少。(2)在三叉神经尾侧核浅层出现的P物质对N-200(有髓纤维的标志物)或IB4(非肽能神经元的标志物)均无免疫反应。这些结果表明，新生儿辣椒素治疗会导致长期的免疫缺陷2.行为学研究：长期观察精神神经部分损伤后机械触觉阈值的变化：(1)小鼠神经损伤后机械触觉阈值明显升高，这种状态持续1周左右；(2)这种阈值的升高在1周左右下降，并维持在较高的阈值水平4周。本动物模型阈值的变化与临床观察的周围神经损伤相似，提示周围神经损伤与Vc传入末梢的神经肽有关，神经损伤后感觉障碍的发生机制及其恢复与神经肽的变化有一定关系。

1.Immuno-histochemical study : Temporo-spatial changes of substance P distribution in the trigeminal caudalis after nerve injury(1)Neonatal capsaicin treatment induces a disappearance of substance p in deep part of the trigeminal caudalis (Vc) in adult and a transient decrease of substance p in superficial layers of the Vc recovered at 2 weeks of age.(2)This emerged substance p in superficial layers of the Vc does not have any immunoreactivity either for N-200 (the marker for myelinated fiber) or IB4 (the marker for non-peptidergic neuron).These results suggest that neonatal capsaicin treatment induces a long term deficit in nociceptive transmission in the Vc and it is caused by unavailability of neurotransmitter releasing but not by an disappearance of neural transmitters.2.Behavioral study : Long term observation of changes in the mechanical-touch threshold after partial injury of mental nerve(1)Ligation of the mental nerve in mice induces an apparent elevation of mechanical touch threshold just after nerve injury and this state lasts for 1 week.(2)This elevation of the threshold decreases around 1 weeks and relative high level of the threshold remains for 4 weeks. After that, this elevation decreases and reaches to the control level.(3)Changes in the threshold of this animal model look similar to clinical observation of peripheral nerve injury.Combined with these results, it was suggested that peripheral nerve injury relates to neuropeptide from the afferent terminals in the Vc and mechanism for sensory impairment following nerve injury and its recovery has some relationships to change in the neuropeptide.