Bondareff W
Mech Ageing Dev. 1980 Mar;12(3):221-9. doi: 10.1016/0047-6374(80)90044-5.
A portentous reorganization of the dentate gyrus occurs characteristically in senescent rats. This reorganization includes atrophy of dendrites, hypertrophy of astrocytes and a 27% loss of axodendritic synapses in the molecular layer of the dentate gyrus. A coincident loss of axosomatic synapses is now reported. These synapses on granule cell somata were counted in electron micrographs of representative coronal sections through the dentate gyri of five 3-month-old and five 25-month-old Fischer-344 male rats. A 15% decrease in the number of axosomatic synapses per 100 micron length of granule cell plasma membrane and a 22% decrease in the amount of neuronal surface covered by synapses were found in the senescent, as compared with the young adult, animals. These differences were statistically significant. As synapses on granule cell somata are inhibitory terminals of GABAergic interneurons it is suggested that their loss in senescence may be compensatory for the loss of axodendritic synapses, which are excitatory. By means of a compensatory loss of synapses it may be possible for the aging animal to maintain a reasonably adaptive level of function in spite of ongoing changes in the level of granule cell excitation resulting from the reorganization of the dentate gyrus in senescence.
齿状回的一种显著重组特征性地发生在衰老大鼠中。这种重组包括树突萎缩、星形胶质细胞肥大以及齿状回分子层中轴-树突触减少27%。现在报告了轴-体突触的同步减少。在五只3个月大及五只25个月大的Fischer-344雄性大鼠齿状回的代表性冠状切片电子显微照片中,对颗粒细胞胞体上的这些突触进行了计数。与年轻成年动物相比,衰老动物每100微米颗粒细胞质膜长度上的轴-体突触数量减少了15%,突触覆盖的神经元表面积减少了22%。这些差异具有统计学意义。由于颗粒细胞胞体上的突触是GABA能中间神经元的抑制性终末,因此有人提出,它们在衰老过程中的丧失可能是对兴奋性轴-树突触丧失的一种代偿。通过突触的代偿性丧失,衰老动物尽管由于衰老过程中齿状回重组导致颗粒细胞兴奋水平不断变化,但仍有可能维持合理的适应性功能水平。