The term Fetal Alcohol Spectrum Disorder (FASD) includes a group of diseases caused by fetal exposure to alcohol (FAE). FASD patients display heterogenous socio-emotional and cognitive deficits, particularly in the domain of executive function, which share symptoms with other neuropsychiatric disorders. Despite the availability of several preclinical models, the developmental brain defects causally linked to behavioral deficits induced by FAE remain poorly understood. Here, we first review the FAE-induced synaptic and circuit impairments in mesocorticolimbic areas involved in social and motor behaviors. Then, we consider the effects of FAE on cortical excitation/inhibition balance and its impact on both corticostriatal pathway function and cognitive abilities. In particular, we propose three non-mutually exclusive circuit models of corticostriatal dysfunctions to account for some of the FAE-induced cognitive deficits. One model posits that associative-sensorimotor imbalance causes hyper goal-directed behavior and a second model implies that alteration of prefrontal-striatal behavioral suppression circuits results in the loss of behavioral inhibition. A third model suggests that local striatal circuit deficits affect striatal neuronal ensemble function to impair action selection and performance. Finally, we discuss how pre-clinical approaches suggest potential rescue strategies for neuronal circuit defects in FASD patients.