Department of Neuroscience and Brain Technologies, Italian Institute of Technology, Genova, Italy.
Epilepsia. 2010 Jul;51 Suppl 3:61-5. doi: 10.1111/j.1528-1167.2010.02612.x.
Extracellular matrix (ECM) in the brain is composed of molecules synthesized and secreted by neurons and glial cells, which form stable aggregates of diverse composition in the extracellular space. In the mature brain, ECM undergoes a slow turnover and restrains structural plasticity while supporting multiple physiologic processes, including perisomatic gamma-aminobutyric acid (GABA)ergic inhibition, synaptic plasticity, and homeostatic regulations. Seizures lead to striking remodeling of ECM, which may be essentially engaged in different aspects of epileptogenesis. This view is supported by human genetic studies linking ECM molecules and epilepsy, by data showing altered epileptogenesis in mice deficient in ECM molecules, and by evidence that ECM may shape seizure-induced sprouting of mossy fibers, granule cell dispersion, and astrogliosis. Therefore, restraining seizure-induced remodeling of ECM or suppressing the signaling triggered by the remodeled ECM might provide effective therapeutic strategies to antagonize the progression of epileptogenesis.
脑外细胞基质（ECM）由神经元和神经胶质细胞合成和分泌的分子组成，在细胞外空间形成多种成分的稳定聚集体。在成熟的大脑中，ECM 经历缓慢的更替，在支持多种生理过程的同时限制结构可塑性，包括胞体 GABA 能抑制、突触可塑性和动态平衡调节。癫痫发作导致 ECM 显著重塑，可能主要参与癫痫发生的不同方面。这一观点得到了人类遗传研究的支持，这些研究将 ECM 分子与癫痫联系起来，也得到了数据的支持，这些数据显示 ECM 分子缺失的小鼠癫痫发生改变，还有证据表明 ECM 可能塑造癫痫诱导的苔藓纤维出芽、颗粒细胞分散和星形胶质细胞增生。因此，抑制癫痫诱导的 ECM 重塑或抑制重塑 ECM 触发的信号可能为对抗癫痫发生提供有效的治疗策略。
