Ethanol, a teratogenic molecule, affects the development and the maturation of the central nervous system from fetal life until the end of adolescence. Exposure to alcohol during fetal life causes irreversible deficits in learning. During adolescence, Binge Drinking alcohol abuse also induces memory loss. However, the cellular mechanisms in these two contexts are still unclear. The hippocampus, a brain structure, is involved in memory and learning through synaptic plasticity phenomena between neurons. Here, we investigated the effects of ethanol i) during fetal life and ii) in adolescence on synaptic plasticity in teenage rat hippocampus using electrophysiological techniques, pharmacology and biochemistry. We show that glutamate and GABA are strongly involved in the long-term disruption of synaptic plasticity after fetal alcohol. During adolescence, only the glutamate is disrupted after a binge drinking episode, resulting in rapid and prolonged abolition of synaptic plasticity and learning deficits. Interestingly, bumetanide, a diuretic, restores disturbances after fetal alcohol. Ethanol during brain development disrupts learning by inducing an imbalance between excitation and inhibition in the neural network of the hippocampus