Computer model of antiepileptic effects mediated by alterations in GABAA‐mediated inhibition
作者:
Elizabeth Thomas,
William Lytton,
期刊:
NeuroReport
(OVID Available online 1998)
卷期:
Volume 9,
issue 4
页码: 691-696
ISSN:0959-4965
年代: 1998
出版商: OVID
关键词: Absence epilepsy;GABAA;Synchrony;Thalamus
数据来源: OVID
摘要:
RESULTS from a computer model of a thalamic network predict that agents augmenting GABAA-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.
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