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首页> 外文期刊>Journal of Neurophysiology >Neonatal infraorbital nerve crush-induced CNS synaptic plasticity and functional recovery
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Neonatal infraorbital nerve crush-induced CNS synaptic plasticity and functional recovery

机译：新生儿缺虫神经挤压诱导的CNS突触塑性和功能恢复

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Infraorbital nerve (ION) transec-tion in neonatal rats leads to disruption of whisker-specific neural patterns (barrelettes), conversion of functional synapses into silent synapses, and reactive gliosis in the brain stem trigeminal principal nucleus (PrV). Here we tested the hypothesis that neonatal peripheral nerve crush injuries permit better functional recovery of associated central nervous system (CNS) synaptic circuitry compared with nerve transection. We developed an in vitro whisker pad-trigeminal ganglion (TG)-brain stem preparation in neonatal rats and tested functional recovery in the PrV following ION crash. Intracellular recordings revealed that 68% of TG cells innervate the whisker pad. We used the proportion of whisker pad-innervating TG cells as an index of ION function. The ION function was blocked by ~64%, immediately after mechanical crash, then it recovered beginning after 3 days postinjury and was complete by 7 days. We used this reversible nerve-injury model to study peripheral nerve injury-induced CNS synaptic plasticity. In the PrV, the incidence of silent synapses increased to -3.5 times of control value by 2-3 days postinjury and decreased to control levels by 5-7 days postinjury. Peripheral nerve injury-induced reaction of astrocytes and microglia in the PrV was also reversible. Neonatal ION crash disrupted barrelette formation, and functional recovery was not accompanied by de novo barrelette formation, most likely due to occurrence of recovery postcritical period (P3) for pattern formation. Our results suggest that nerve crash is more permissive for successful regeneration and reconnection (collectively referred to as "recovery" here) of the sensory inputs between the periphery and the brain stem.
机译：新生儿大鼠的眶下神经（离子）转基因导致晶须特异性神经图案（鼠李）的破坏，官能突触转化为静音突触，脑茎三叉原理核（PRV）中的反应性脊髓源。在这里，我们测试了新生儿周围神经压榨损伤的假设允许与神经横断相比，新生儿周围神经压榨损伤允许更好的相关中枢神经系统（CNS）突触电路的功能恢复。我们在新生大鼠中开发了一种体外晶须垫 - 三叉神经节（Tg）-Brain干燥制剂，并在离子碰撞后的PRV中测试功能恢复。细胞内记录显示，68％的TG细胞接管晶须垫。我们使用了晶须垫接收TG细胞的比例作为离子功能的指标。在机械碰撞后立即将离子功能堵塞〜64％，然后在Postinjury 3天后开始恢复，并完成7天。我们使用这种可逆神经损伤模型来研究周围神经损伤诱导的CNS突触可塑性。在PRV中，静音突触的发生率增加到-3.5倍的控制价值，在第2-3天内，下午2-3天减少5-7天的控制水平。周围神经损伤诱导的星形胶质细胞和微胶质中PRV的反应也是可逆的。新生儿离子崩溃扰乱了枪管形成，并且功能性回收不伴随着De Novo Barlelette的形成，很可能是由于恢复后期（P3）的模式形成。我们的研究结果表明，神经撞击更为允许成功的再生和重新连接（统称为“这里的恢复”脑干之间的感觉输入的“这里”。

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