脊髓背角Ⅱ板层长时程增强诱导及维持过程中的突触形态计量学研究

A quantitative study of the synaptic alterations in spinal dorsal horn during the induction and maintenance of long-term potentiation

本研究用体视学方法探讨了在C纤维诱发电位长时程增强(long-term potentiation,LTP)的诱导及维持过程中的脊髓背角Ⅱ板层的突触形态变化。结果显示:(1)在LTP形成后30min,Ⅱ板层内的突触后致密物质(postsynaptic density,PSD)增厚,突触间隙增宽;(2)在LTP形成后3h,PSD厚度、突触间隙宽度及突触界面曲率都有明显增加;(3)在LTP诱导和维持全过程中,总突触的数密度比对照组有明显增高。(4)在LTP形成后3h和5h,穿孔性突触的数密度与对照组比较有明显增高。上述结果显示:PSD增厚是LTP诱导阶段的主要形态学变化。突触界面曲率增大及穿孔突触数目增多是LTP维持阶段的主要形态学基础。

By using stereological morphometric techniques, we examined the ultrastructure of synapses in lamine Ⅱ of the spinal dorsal horn of Sprague Dawley rats 30 min, 3 h and 5 h after long-term potentiation (LTP) induction. We found that the numerical density per unit volume (Nv) of total synapses, the thickness of the postsynaptic density (PSD), width of the synaptic cleft increased significantly after the establishment of LTP. (1) Thirty minutes after the formation of LTP, the thickness of the PSD increased from 0.029±0.0064μm (control) to 0.036±0.009μm (P<0.05) and the width of the synaptic cleft increased from 0.0181±0.0024 μm (control) to 0.0197±0.0029μm (P< 0.05); the number of synaptic vesicles decreased from 0.122±0.0l1/μm^2 to 0.085±0.010μm^2 (P<0.05); (2) 3 h after the formation of LTP, the thickness of PSD and the width of the synaptic cleft had no difference compared with those 30 min after LTP. The number of synaptic vesicles increased from 0.122±0.011/μm^2 to 0.138±0.015/μm^2; the curvature of the synaptic interface increased from 1.153±0.195 to 1.386 ±0.311 (P<0.05, compared with control). Nv of negative synapses increased from 0.0187±0.0056 to 0.0543±0.0152 (P<0.05, compared with control), Nv of perforated synapses also increased from 0.0135±0.0053 to 0.0215±0.0076 (P<0.05, compared with control). These data suggest that the increase in thickness of PSD might be the major morphological change during the indution of LTP, while the increase in curvature of the synaptic interface, and the number of perforated synapses might be responsible for the maintenance of the spinal LTP.