et al., 2000). In addition, new connections in the cortex are generated when monkeys learn a new skill, such as using a tool, or after localized brain damage (Dancause, Barbay, et al., 2005; Hihara, Notoya, et al., 2006; Johansen-Berg, 2007). Similarly, the learning of new skills in humans leads to changes in the cortical regions that subserve that task (Doyon and Benali, 2005; Ungerleider, Doyon, and Karni, 2002).
One emerging question in the study of neural plasticity is the role that newly generated neurons may have in the postnatal brain. Mature, differentiated neurons have generally lost the capacity to divide to produce new cells, and a central dogma in neuroscience for most of the past century has been that all proliferation of new neurons ends during fetal life. However, many studies have recently provided indisputable evidence that postnatal production of new neurons, or neurogenesis, does in fact occur, even in adult life, in a small number of brain regions and in a large range of species (Gould, 2007). These neurons are generated from a population of neural stem cells that are retained in the brain. Although the full range of triggers for neurogenesis has yet to be identified, it appears to include a broad array of stimuli from experience and the environment, including physical activity and even antidepressant medications (Lledo, Alonso, and Grubb, 2006). The birth of new neurons in postnatal life is one of many means through which experience can modify anatomical circuitry and functional activity in the brain. The number of new neurons generated is small, however, and whether and to what extent these neurons are able to integrate into synaptic circuits and exert a significant functional influence in the brain are at present unclear (Ghashghaei, Lai, and Anton, 2007; Gould, 2007; Lledo, Alonso, and Grubb, 2006).
The ongoing capacity for change in the brain underlies potential mechanisms through which brain function can compensate for, or even recover from, a disorder, whether that disorder derives primarily from adverse genetic or environmental influences or a combination of both. In a broad sense, then, virtually all responses in the brain that help compensate for the presence of a disorder can be considered neuroplastic responses, and they are likely to have their structural basis in the remodeling of synaptic connections and neural systems in the brain. Moreover, the causes of certain MEB disorders are thought to involve the exaggeration or “hijacking” of certain learning and memory processes. This is thought to be a prominent feature of the pathogenesis of addictive disorders, for example, in which substances of abuse pharmacologically induce plasticity in brain circuits that are involved in reward and associative learning. This exaggerated plasticity helps establish new, abnormal stimulus–response associations among the substance, the cues that accompany it, and the behavioral responses to those cues that define disorders of addiction (Kalivas and O’Brien, 2008; Kauer and Malenka, 2007).