癫癎突触可塑性的研究动态

Dynamic Process of Synaptic Plasticity in Epilepsy

癫癎的形成与大脑神经元之间异常突触联系和病理性神经环路的建立而导致的兴奋性增强有关,这些异常突触联系和病理性神经环路也是突触可塑性的表现。通过癫癎点燃动物模型、癫癎状态和癫癎形成机制的研究表明,长时程增强(LTP)、NF-κB基因调控蛋白、苔藓纤维出芽(MFS)、神经肽Y(NPY)、NCAM以及谷氨酸受体NMDA型和KA型等,均参与神经元突触可塑性的过程,在癫癎的发生机制中起着重要作用。

The formation of epilepsy is attributable to the abnormal synaptic connections between cerebral neuronal cells and the pathological neuro circuit which finally contribute to enhanced synaptic excitability. Accumulating evidence using amygdaloid kindling rat model has shown that long term potentiation（LTP）, NF-kappaB pro rein, mossy fiber sprouting（MFS）, neuropeptide Y（NPY）, neural cell adhesion molecule（NCAM） and glutamate receptors（NMDA and KA） participate in the process of synaptic plasticity and play important roles in epileptic pathophysiology.