Leite João Pereira, Neder Luciano, Arisi Gabriel Maisonnave, Carlotti Carlos Gilberto, Assirati João Alberto, Moreira Jorge Eduardo
Department of Neurology, University of São Paulo School of Medicine at Ribeirão Preto, São Paulo, Brazil.
Epilepsia. 2005;46 Suppl 5:134-41. doi: 10.1111/j.1528-1167.2005.01021.x.
Central nervous system synapses have an intrinsic plastic capacity to adapt to new conditions with rapid changes in their structure. Such activity-dependent refinement occurs during development and learning, and shares features with diseases such as epilepsy. Quantitative ultrastructural studies based on serial sectioning and reconstructions have shown various structural changes associated with synaptic strength involving both dendritic spines and postsynaptic densities (PSDs) during long-term potentiation (LTP). In this review, we focus on experimental studies that have analyzed at the ultrastructural level the consequences of LTP in rodents, and plastic changes in the hippocampus of experimental models of epilepsy and human tissue obtained during surgeries for intractable temporal lobe epilepsy (TLE). Modifications in spine morphology, increases in the proportion of synapses with perforated PSDs, and formation of multiple spine boutons arising from the same dendrite are the possible sequence of events that accompany hippocampal LTP. Structural remodeling of mossy fiber synapses and formation of aberrant synaptic contacts in the dentate gyrus are common features in experimental models of epilepsy and in human TLE. Combined electrophysiological and ultrastructural studies in kindled rats and chronic epileptic animals have indicated the occurrence of seizure- and neuron loss-induced changes in the hippocampal network. In these experiments, the synaptic contacts on granule cells are similar to those described for LTP. Such changes could be associated with enhancement of synaptic efficiency and may be important in epileptogenesis.
中枢神经系统突触具有内在的可塑性,能够通过其结构的快速变化来适应新环境。这种依赖于活动的精细化过程发生在发育和学习期间,并且与癫痫等疾病具有共同特征。基于连续切片和重建的定量超微结构研究表明,在长时程增强(LTP)过程中,涉及树突棘和突触后致密物(PSD)的各种结构变化与突触强度相关。在这篇综述中,我们重点关注在超微结构水平上分析啮齿动物LTP后果、癫痫实验模型海马体中的可塑性变化以及难治性颞叶癫痫(TLE)手术中获取的人体组织的实验研究。脊柱形态的改变、具有穿孔PSD的突触比例增加以及同一树突产生多个脊柱终扣是伴随海马体LTP的可能事件序列。苔藓纤维突触的结构重塑以及齿状回中异常突触接触的形成是癫痫实验模型和人类TLE的共同特征。对点燃大鼠和慢性癫痫动物进行的电生理和超微结构联合研究表明,癫痫发作和神经元丢失会导致海马体网络发生变化。在这些实验中,颗粒细胞上的突触接触与LTP中描述的相似。这种变化可能与突触效率的提高有关,并且在癫痫发生过程中可能很重要。