G-protein activation kinetics and spill-over of GABA may account for differences between inhibitory responses in the hippocampus and thalamus.
Alain Destexhe and Terrence J. Sejnowski

Proceedings of the National Academy of Sciences of the United States of America 92: 9515-9519, 1995.

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We have developed a model of GABAergic synaptic transmission mediated by GABA(A) and GABA(B) receptors, including cooperativity in the G-protein cascade mediating the activation of K+ channels by GABA(B) receptors. If the binding of several G-proteins is needed to activate the K+ channels, then only a prolonged activation of GABA(B) receptors evoked detectable currents. This could occur if strong stimuli evoked release in adjacent terminals, and the spill-over resulted in the prolonged activation of the receptors, leading to inhibitory responses similar to those observed in hippocampal slices. The same model also reproduced thalamic GABA(B) responses to high-frequency bursts of stimuli. In this case, the prolonged activation of the receptors was due to high-frequency release conditions. This model provides new insights into the function of GABA(B) receptors in normal and epileptic discharges.