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Can GABA A conductances explain the fast oscillation frequency of absence seizures in rodents?
Author(s) -
Destexhe Alain
Publication year - 1999
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1999.00660.x
Subject(s) - neuroscience , gabaa receptor , gabaergic , oscillation (cell signaling) , physics , spike and wave , gabab receptor , gamma aminobutyric acid , electrophysiology , epilepsy , biology , receptor , inhibitory postsynaptic potential , genetics , biochemistry
Rodent models of absence epilepsy generate spike‐and‐wave oscillations at relatively fast frequency (5–10 Hz) compared with humans (≈ 3 Hz). Possible mechanisms for these oscillations were investigated by computational models that included the complex intrinsic firing properties of thalamic and cortical neurons, as well as the multiple types of synaptic receptors mediating their interactions. The model indicates that oscillations with spike‐and‐wave field potentials can be generated by thalamocortical circuits. The frequency of these oscillations critically depended on GABAergic conductances in thalamic relay cells, ranging from 2–4 Hz for strong GABA B conductances to 5–10 Hz when GABA A conductances were dominant. This model therefore suggests that thalamocortical circuits can generate two types of spike‐and‐wave oscillations, whose frequency is determined by the receptor type mediating inhibition in thalamic relay cells. Experiments are proposed to test this mechanism.