Brandão F, Paula-Barbosa M M, Cadete-Leite A
Department of Anatomy, Porto Medical School, Portugal.
Alcohol. 1995 May-Jun;12(3):279-88. doi: 10.1016/0741-8329(94)00107-o.
In previous studies we have demonstrated that prolonged ethanol consumption induced hippocampal neuronal loss. In addition, we have shown that withdrawal after chronic alcohol intake augmented such degenerative activity leading to increased neuronal death in all subregions of the hippocampal formation but in the CA3 field. In an attempt to reverse this situation, we tested, during the withdrawal period, the effects of piracetam (2-oxo-1-pyrrolidine acetamide), a cyclic derivative of gamma-aminobutyric acid, as there is previous evidence that it might act as a neuronoprotective agent. The total number of dentate granule, hilar, and CA3 and CA1 pyramidal cells of the hippocampal formation were estimated using unbiased stereological methods. We found out that in animals treated with piracetam the numbers of dentate granule, hilar, and CA1 pyramidal cells were significantly higher than in pure withdrawn animals, and did not differ from those of alcohol-treated rats that did not undergo withdrawal. These data suggest that piracetam treatment impedes, during withdrawal, the pursuing of neuronal degeneration.
在先前的研究中，我们已经证明长期摄入乙醇会导致海马神经元丢失。此外，我们还表明，长期饮酒后戒断会加剧这种退行性活动，导致海马结构所有亚区（但CA3区除外）的神经元死亡增加。为了扭转这种情况，在戒断期间，我们测试了γ-氨基丁酸的环状衍生物吡拉西坦（2-氧代-1-吡咯烷乙酰胺）的作用，因为之前有证据表明它可能作为一种神经保护剂。使用无偏倚的体视学方法估计海马结构中齿状颗粒细胞、门区细胞以及CA3和CA1锥体细胞的总数。我们发现，用吡拉西坦治疗的动物中，齿状颗粒细胞、门区细胞和CA1锥体细胞的数量显著高于单纯戒断的动物，且与未戒断的酒精处理大鼠的细胞数量没有差异。这些数据表明，吡拉西坦治疗在戒断期间可阻止神经元变性的继续发展。
