Breakdown of GABAergic Control in Thalamocortical Epilepsies

Peter Klein
Absence epilepsy, characterized by brief seizures that spread throughout the brain, results from abnormal rhythmic activity between networks of thalamic and cortical neurons. Inhibitory GABAergic signaling among neurons of the reticular thalamic (RT) nucleus is proposed to form a critical choke point that normally prevents the generation of seizures. Neurons need to maintain low intracellular Cl- concentrations ([Cl-]i) to enable inhibitory neuronal responses to GABAA receptor-mediated signaling. The Cl- transporter KCC2 and extracellular impermeant anions...
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