The developing brain, and to a lesser extent the adult brain, have evolved mechanisms to take advantage of experience normally available in history of the species, or "expected" in the organism's normal environment. Basic sensory development, for example, typically requires sensory experience for normal development. A mechanism often used for this experience-expectant aspect of development is overproduction of synapses followed by selective pruning of those not stabilized or preserved by experience. Later in development, experiences occur that cannot have been anticipated by natural selection. Evidence suggests that these "experience dependent" kinds of information may be encoded, at least in part, by the formation of new synapses, as occurs in rats exposed to an enriched environment. In addition to encoding specific memories, this synapse formation is shown to contribute to recovery from brain injury. While the plasticity of overproduction and pruning may be limited to a brief part of life and hence constitutes a critical or sensitive period phenomenon, the ability to generate new synapses appears to continue throughout life and hence to serve as a basis for resilience or recovery from disruptive events in early development. We have demonstrated that in an animal model of Fetal Alcohol Syndrome (FAS) specifically targeting binge-like drinking during the third trimester of pregnancy the damage to cerebellum and motor cortex was permanent and associated with behavioral deficits that lasted long after the exposure to alcohol was over. Nevertheless, when animals were trained on a complex motor learning task, the outcome was lasting improvement in behavioral skills and increased synaptogenesis in both cerebellar and motor cortices. These results suggest that such intervention can serve as a component of a rehabilitative program to enhance brain function that has been impaired by alcohol exposure.