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Epilepsy is a common neurological disorder characterized by recurrent seizures. Most antiepileptic drugs (AEDs) work by regulating the balance of the excitatory glutamatergic and inhibitory GABAergic transmission. However, the current AEDs cannot successfully control seizures in most ([70%) patients with temporal lobe epilepsy (TLE)[1], in whom seizures typically begin in the hippocampus. This may be caused by changes in the synaptic efficacy and remodeling of neural circuits, such as alterations in the distribution/expression of GABAA receptor subunits and mossy-fiber sprouting. Since Dr. Karen Gale and colleagues originally described the seizure-modulating effects of nigral GABAergic transmission in the early 1980s [2], the substantia nigra pars reticulata (SNpr) has been considered an important seizure-modulating area. For example, lesioning or pharmacological inhibition of the SNpr suppresses seizures …