Bundman M C, Gall C M
Department of Anatomy and Neurobiology, University of California, Irvine 92717.
Hippocampus. 1994 Oct;4(5):611-22. doi: 10.1002/hipo.450040511.
Hilus lesion-induced recurrent limbic seizures cause a dramatic increase in the numbers of somatic spines on dentate gyrus granule cells in the adult rat. Somatic spines are maximally increased 3 h after the initiation of seizures at which time many of these spines form synapses. The present quantitative electron microscopic study assessed the numbers and types of synapses present on the granule cell perikarya and somatic spines of control and experimental seizure rats with the goal of determining if newly elaborated somatic spines arise at the site of pre-existing synapses or are associated with new innervation. Experimental rats were sacrificed 5 h after hilar lesion placement (or 3 h after seizure onset). In both control and hilus-lesioned (HL) rats, 15-20% of the somatic spines could be seen to form synaptic contacts within a single plane of section; these synapses were almost exclusively of the asymmetric type. With the increased incidence of spines in experimental-seizure rats, there was a 6.25-fold greater number of spine synapses in HL versus control rats. There was, in addition, a 60% decrease in the number of asymmetric synapses occurring directly on the granule cell perikarya but no change in the total (spine plus somatic) number of asymmetric synapses. Although few asymmetric synapses were associated with spines in control tissue, 60-70% of asymmetric synapses were associated with spines in experimental-seizure tissue. In addition, in hilus lesion rats symmetric somatic synapses were increased by 20% on cells in deep stratum granulosum resulting in a dissolution of the superficial-to-deep innervation gradient present in the untreated rat. These findings support the conclusion that spines induced by seizure activity form at the site of pre-existing asymmetric synapses on the granule cells and demonstrate that brief seizure episodes can rapidly induce marked changes in innervation patterns in the adult brain.
海马损伤诱发的反复性边缘叶癫痫发作会使成年大鼠齿状回颗粒细胞的体细胞棘突数量显著增加。癫痫发作开始后3小时，体细胞棘突数量达到最大值，此时许多棘突形成突触。本定量电子显微镜研究评估了对照大鼠和实验性癫痫发作大鼠颗粒细胞胞体及体细胞棘突上突触的数量和类型，目的是确定新形成的体细胞棘突是出现在预先存在的突触部位，还是与新的神经支配有关。在海马损伤放置后5小时（或癫痫发作开始后3小时）处死实验大鼠。在对照大鼠和海马损伤（HL）大鼠中，在单个切片平面内可看到15 - 20%的体细胞棘突形成突触接触；这些突触几乎都是不对称型的。随着实验性癫痫发作大鼠棘突发生率的增加，HL大鼠的棘突突触数量比对照大鼠多6.25倍。此外，直接出现在颗粒细胞胞体上的不对称突触数量减少了60%，但不对称突触的总数（棘突加体细胞）没有变化。虽然在对照组织中很少有不对称突触与棘突相关，但在实验性癫痫发作组织中，60 - 70%的不对称突触与棘突相关。此外，在海马损伤大鼠中，深层颗粒层细胞上的对称体细胞突触增加了20%，导致未处理大鼠中存在的浅到深的神经支配梯度消失。这些发现支持了癫痫活动诱导的棘突在颗粒细胞上预先存在的不对称突触部位形成的结论，并表明短暂的癫痫发作能迅速诱导成年大脑神经支配模式的显著变化。
