Division Epilepsy, Department of Neurology, Boston Children's Hospital and Harvard Medical School, 300 Longwood Ave, Boston, MA, 02115, USA,
Curr Neurol Neurosci Rep. 2015 May;15(5):27. doi: 10.1007/s11910-015-0545-1.
Traumatic brain injury (TBI) leads to multiple short- and long-term changes in neuronal circuits that ultimately conclude with an imbalance of cortical excitation and inhibition. Changes in neurotransmitter concentrations, receptor populations, and specific cell survival are important contributing factors. Many of these changes occur gradually, which may explain the vulnerability of the brain to multiple mild impacts, alterations in neuroplasticity, and delays in the presentation of posttraumatic epilepsy. In this review, we provide an overview of normal glutamate and GABA homeostasis and describe acute, subacute, and chronic changes that follow injury. We conclude by highlighting opportunities for therapeutic interventions in this paradigm.
创伤性脑损伤（TBI）导致神经元回路的多个短期和长期变化，最终导致皮质兴奋和抑制失衡。神经递质浓度、受体群体和特定细胞存活的变化是重要的促成因素。其中许多变化是逐渐发生的，这可能解释了大脑容易受到多次轻度冲击、神经可塑性改变和外伤性癫痫发作延迟的原因。在这篇综述中，我们提供了对正常谷氨酸和 GABA 动态平衡的概述，并描述了损伤后的急性、亚急性和慢性变化。最后，我们强调了在这一范式中治疗干预的机会。
