PDF(Pubmed)
Abstract：
Posttraumatic epilepsy (PTE) is one of the most critical complications of traumatic brain injury (TBI), significantly increasing TBI patients\' neuropsychiatric symptoms and mortality. The abnormal accumulation of glutamate caused by TBI and its secondary excitotoxicity are essential reasons for neural network reorganization and functional neural plasticity changes, contributing to the occurrence and development of PTE. Restoring glutamate balance in the early stage of TBI is expected to play a neuroprotective role and reduce the risk of PTE.
To provide a neuropharmacological insight for drug development to prevent PTE based on regulating glutamate homeostasis.
We discussed how TBI affects glutamate homeostasis and its relationship with PTE. Furthermore, we also summarized the research progress of molecular pathways for regulating glutamate homeostasis after TBI and pharmacological studies aim to prevent PTE by restoring glutamate balance.
TBI can lead to the accumulation of glutamate in the brain, which increases the risk of PTE. Targeting the molecular pathways affecting glutamate homeostasis helps restore normal glutamate levels and is neuroprotective.
Taking glutamate homeostasis regulation as a means for new drug development can avoid the side effects caused by direct inhibition of glutamate receptors, expecting to alleviate the diseases related to abnormal glutamate levels in the brain, such as PTE, Parkinson\'s disease, depression, and cognitive impairment.
It is a promising strategy to regulate glutamate homeostasis through pharmacological methods after TBI, thereby decreasing nerve injury and preventing PTE.
To provide a neuropharmacological insight for drug development to prevent PTE based on regulating glutamate homeostasis.
We discussed how TBI affects glutamate homeostasis and its relationship with PTE. Furthermore, we also summarized the research progress of molecular pathways for regulating glutamate homeostasis after TBI and pharmacological studies aim to prevent PTE by restoring glutamate balance.
TBI can lead to the accumulation of glutamate in the brain, which increases the risk of PTE. Targeting the molecular pathways affecting glutamate homeostasis helps restore normal glutamate levels and is neuroprotective.
Taking glutamate homeostasis regulation as a means for new drug development can avoid the side effects caused by direct inhibition of glutamate receptors, expecting to alleviate the diseases related to abnormal glutamate levels in the brain, such as PTE, Parkinson\'s disease, depression, and cognitive impairment.
It is a promising strategy to regulate glutamate homeostasis through pharmacological methods after TBI, thereby decreasing nerve injury and preventing PTE.
摘要：
背景：创伤后癫痫（PTE）是创伤性脑损伤（TBI）最关键的并发症之一，显著增加TBI患者的神经精神症状和死亡率。TBI引起的谷氨酸异常积累及其继发性兴奋性毒性是神经网络重组和功能神经可塑性改变的本质原因，有助于PTE的发生和发展。在TBI早期恢复谷氨酸平衡有望发挥神经保护作用，降低PTE的风险。
目的：为基于调节谷氨酸稳态预防PTE的药物开发提供神经药理学见解。
方法：我们讨论了TBI如何影响谷氨酸稳态及其与PTE的关系。此外，总结了TBI后调节谷氨酸稳态的分子途径的研究进展，以及通过恢复谷氨酸平衡预防PTE的药理研究。
结果：TBI可以导致大脑中谷氨酸的积累，这增加了PTE的风险。靶向影响谷氨酸稳态的分子途径有助于恢复正常的谷氨酸水平并且具有神经保护作用。
结论：将谷氨酸稳态调节作为新药开发的手段，可以避免直接抑制谷氨酸受体引起的副作用，期望缓解与大脑中谷氨酸水平异常有关的疾病，比如PTE,帕金森病,抑郁症,和认知障碍。
结论：TBI后通过药理学方法调节谷氨酸稳态是一种有前途的策略，从而减少神经损伤和预防PTE。
目的：为基于调节谷氨酸稳态预防PTE的药物开发提供神经药理学见解。
方法：我们讨论了TBI如何影响谷氨酸稳态及其与PTE的关系。此外，总结了TBI后调节谷氨酸稳态的分子途径的研究进展，以及通过恢复谷氨酸平衡预防PTE的药理研究。
结果：TBI可以导致大脑中谷氨酸的积累，这增加了PTE的风险。靶向影响谷氨酸稳态的分子途径有助于恢复正常的谷氨酸水平并且具有神经保护作用。
结论：将谷氨酸稳态调节作为新药开发的手段，可以避免直接抑制谷氨酸受体引起的副作用，期望缓解与大脑中谷氨酸水平异常有关的疾病，比如PTE,帕金森病,抑郁症,和认知障碍。
结论：TBI后通过药理学方法调节谷氨酸稳态是一种有前途的策略，从而减少神经损伤和预防PTE。
