Computer model of antiepileptic effects mediated by alterations in GABA(A)-mediated inhibition.
Results from a computer model of a thalamic network predict that agents augmenting GABA(A)-mediated inhibition in the reticular thalamic (RE) nucleus will be antiepileptic or desynchronizing. This provides support for the hypothesis that antiepileptics like benzodiazepines may exert their effects through an isolated increase of inhibition in the RE nucleus. When desynchronized, the model thalamocortical neurons showed a decreased probability of firing a low threshold spike, a decreased secondary inhibitory postsynaptic potential and a higher frequency of oscillations. The transition to desynchrony was also accompanied by an increased frequency in the firing of the model RE neurons.
Thomas
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Institut Leon Fredericq, Liège, Belgium.
Lytton
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D000927:Anticonvulsants / Q000494:pharmacology*; D001569:Benzodiazepines / Q000494:pharmacology; D003198:Computer Simulation; D018756:GABA Antagonists / Q000494:pharmacology*; D006801:Humans; D008959:Models, Neurological; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology*; D012154:Reticular Formation / Q000187:drug effects / Q000502:physiology*; D013787:Thalamic Nuclei / Q000187:drug effects / Q000502:physiology*
D000927:Anticonvulsants; D018756:GABA Antagonists; D011963:Receptors, GABA-A; D001569:Benzodiazepines