Some disorders affect single, or at least relatively uniform, neuronal types, but are so dispersed throughout the CNS as to present problems of delivery. In particular, several types of primary epilepsies may derive from deficits in GABAergic interneuronal numbers and function. GABAergic neurons comprise a plethora of phenotypes, but all share a common transmitter and most derive from a common developmental source in the medial ganglionic eminence (MGE). As such, a number of investigators have asked whether the transplantation of healthy donor interneurons into epileptic cortex may provide benefit to medication-refractory epileptics (Hunt et al., 2013; Southwell et al., 2014). This potential treatment strategy was made possible by the significant migration competence of these cells in the adult cortex, a vestige of their longdistance migration in early development (Wichterle et al., 1999) - a feature shared by glial progenitors, another highly migratory, MGE-derived phenotype similarly amenable to treating diffuse disease. The recent development of protocols appropriate for the production of GABAergic interneurons from human ES and iPS cells (Liu et al., 2000; Maroof et al., 2013) should now enable the assessment of interneuronal transplantation as an approach towards seizure control, using a clinically-realistic cell source.
