Mileusnić R, Veskov R, Rakić L
Life Sci. 1986 Mar 31;38(13):1171-8. doi: 10.1016/0024-3205(86)90171-2.
Effect of electroconvulsive shock on rat brain tubulin content was studied during maturation and aging. The results show that electroconvulsive shock had no effect on soluble tubulin in different brain structures of young animals (22 days) while the same treatment produced a marked decline in adult (95 days) and aged (490-511 days) animals. The same treatment produced inhibition of 3H-leucine incorporation into tubulin and decrease of 3H-colchicine binding in the proteins of synaptosomes isolated from the centricephalic structures of all the ages examined. Tubulin biosynthesis by free polysomes was not diminished to the extent which could explain the decrease of tubulin level found in the soluble or synaptosomal fraction. Thus, our results suggest that changes in soluble tubulin content in response to electroconvulsive shock could be a reflection of changes in equilibrium: tubulin dimers--microtubules--membrane-bound tubulin.
研究了电惊厥休克对大鼠脑微管蛋白含量在成熟和衰老过程中的影响。结果表明,电惊厥休克对幼龄动物(22天)不同脑结构中的可溶性微管蛋白没有影响,而相同处理在成年(95天)和老龄(490 - 511天)动物中导致显著下降。相同处理抑制了3H - 亮氨酸掺入微管蛋白,并降低了从所有检查年龄的中脑结构分离的突触体蛋白中3H - 秋水仙碱的结合。游离多核糖体的微管蛋白生物合成减少的程度不足以解释在可溶性或突触体部分中发现的微管蛋白水平的下降。因此,我们的结果表明,电惊厥休克引起的可溶性微管蛋白含量变化可能反映了平衡的变化:微管蛋白二聚体 - 微管 - 膜结合微管蛋白。