Abstract

Systemic administration of pilocarpine to rats induces seizures that resemble complex partial epilepsy in humans. Susceptibility to these seizures is increased by lesion of the GABAergic striatonigral projection. Transplantation of fetal GABAergic neurons, but also of control non-GABAergic tissue, to the deafferented substantia nigra can reduce such lesion-increased seizure susceptibility. These observations are consistent with prior evidence that GABAergic basal ganglia outflow plays an important role in controlling the spread of seizures, and raise the possibility that intracerebral grafts may be use for therapy of medically-unresponsive epilepsies.

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