Dymecki J, Medyńska E, Walski M
Exp Pathol. 1982;22(2):73-83. doi: 10.1016/s0232-1513(82)80028-5.
In view of the inhibitory influence of ethanol on synaptic transmission demonstrated by numerous authors, the present investigations were undertaken with the purpose of ascertaining the ultrastructural changes in the cholinergic axon terminals of the CNS caused by chronic ethanol intoxication. The experiments were made with 12 rats receiving ethanol according to RATCLIFFE'S model (1972) in increasing doses over a period of 1, 2 and 3 months. The studies comprised evaluation of the electronmicroscopic picture of synapses from the temporal cortex and morphometric analysis of the number of synaptic vesicles in the boutons, of the surface area of synapse cross sections and the surface area of the cross sections of mitochondria in the boutons. Morphometric analysis showed that chronic administration of ethanol to rats reduces the number of synaptic vesicles in the boutons, which may be caused by chronic excitation of neurons by ethanol. Impairment of mitochondria within the synaptic boutons was also noted, probably due to disturbances in cell respiration produced by ethanol. Polymorphism of synaptic vesicles was observed in the form of greatly enlarged ones. It may be interpreted as the morphological manifestation of the process of axon terminals degeneration. Moreover, planimetric analysis demonstrated a significantly increased surface area of synaptic bouton cross sections in all experimental rats as compared with the control ones. The dynamics of the observed changes was not uniform. The reduction of the number of synaptic vesicles and impairment of mitochondria were most pronounced in the early phase of intoxication. In the later period in spite of increased doses and prolonged time of ethanol treatment the changes became rather less intensive, this probably being connected with the process of adaptation. Polymorphism of the synaptic vesicles became more pronounced gradually in the successive experimental groups, probably with corresponding advancing degeneration of the axon terminals. The significantly enlarged surface area of the synaptic boutons cross sections did not show any dependence on the connection of ethanol and duration of its administration.
鉴于众多作者所证实的乙醇对突触传递的抑制作用,本研究旨在确定慢性乙醇中毒导致的中枢神经系统胆碱能轴突终末的超微结构变化。实验选用12只大鼠,按照拉特克利夫(1972年)的模型,在1、2和3个月的时间内逐渐增加乙醇剂量。研究包括对颞叶皮质突触的电子显微镜图像评估,以及对轴突终扣中突触小泡数量、突触横截面表面积和轴突终扣中线粒体横截面表面积的形态计量分析。形态计量分析表明,对大鼠长期给予乙醇会减少轴突终扣中突触小泡的数量,这可能是由于乙醇对神经元的慢性刺激所致。还观察到突触终扣内线粒体受损,可能是由于乙醇引起的细胞呼吸紊乱。观察到突触小泡呈多态性,表现为显著增大。这可能被解释为轴突终末变性过程的形态学表现。此外,平面测量分析表明,与对照组相比,所有实验大鼠的突触终扣横截面表面积均显著增加。观察到的变化动态并不一致。突触小泡数量的减少和线粒体的损伤在中毒早期最为明显。在后期,尽管乙醇剂量增加且治疗时间延长,但变化强度反而降低,这可能与适应过程有关。在连续的实验组中,突触小泡的多态性逐渐变得更加明显,可能伴随着轴突终末相应的渐进性变性。突触终扣横截面表面积的显著增大与乙醇的摄入量及其给药持续时间无关。