Modifications in number and morphology of dendritic spines resulting from chronic ethanol consumption and withdrawal: a Golgi study in the mouse anterior and posterior hippocampus.

Using Golgi-impregnated mice brains, the effects of 2.5, 6.5, and 9.5 months of chronic ethanol consumption were investigated with regard to morphology and number of dendritic spines of CA1 hippocampal pyramidal neurons. The posterior part of the hippocampus was more sensitive to the effects of ethanol consumption than the anterior one. In the posterior part of the structure, the number of dendritic spines was reduced by 25 and 33% after 6.5 and 9.5 months of treatment, respectively, as compared to age-matched controls. Moreover, the remaining spines appeared shorter than normal. After 9 months of ethanol treatment followed by 0.5, 1, and 2 months of withdrawal, the number of dendritic spines was reduced by 24, 19, and 7.5% in the posterior hippocampus, respectively. In the anterior part of the hippocampus, a significant loss of dendritic spines (-20.5%) was observed only after 9.5 months of ethanol consumption. After 1 month of withdrawal, both number and morphology of dendritic spines appeared normal in the anterior hippocampus. These results demonstrate that chronic alcohol consumption leads to morphological alterations and loss of dendritic spines in the hippocampus. However, both dendritic spine number and morphology progressively return to normal values after 2 months of withdrawal. This phenomenon is another example of neuronal plasticity in adult animal brain.