Rodent models of absence epilepsy generate spike-and-wave oscillations at r
elatively fast frequency (5-10 Hz) compared with humans (approximate to 3 H
z). Possible mechanisms for these oscillations were investigated by computa
tional models that included the complex intrinsic firing properties of thal
amic and cortical neurons, as well as the multiple types of synaptic recept
ors mediating their interactions, The model indicates that oscillations wit
h spike-and-wave field potentials can be generated by thalamocortical circu
its. The frequency of these oscillations critically depended on GABAergic c
onductances 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 mode
l therefore suggests that thalamocortical circuits can generate two types o
f spike-and-wave oscillations, whose frequency is determined by the recepto
r type mediating inhibition in thalamic relay cells. Experiments are propos
ed to test this mechanism.