PIRACETAM IMPEDES HIPPOCAMPAL NEURONAL LOSS DURING WITHDRAWAL AFTER CHRONIC ALCOHOL INTAKE

In previous studies we have demonstrated that prolonged ethanol consum ption induced hippocampal neuronal loss. In addition, we have shown th at 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 o f piracetam (2-oxo-1-pyrrolidine acetamide), a cyclic derivative of ga mma-aminobutyric acid, as there is previous evidence that it might act as a neuronoprotective agent. The total number of dentate granule, hi lar, 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 withdra wn animals, and did not differ from those of alcohol-treated rats that did not undergo withdrawal. These data suggest that piracetam treatme nt impedes, during withdrawal, the pursuing of neuronal degeneration.