(Richerson, 2004). Tonic receptors are activated by micromolar levels of the extra-synaptic GABA, which arrives either by diffusion from a synapse before reuptake, or by release into the extracellular space via non-synaptic mechanisms. Tonic GABA receptors may play an important role in epilepsy. On the one hand, reduction of tonic GABA currents (as produced experimentally by a mutation in the delta-subunit of tonic GABA receptors) is associated with generalized epilepsy. On the other hand, progesterone-derived neurosteroids enhance tonic GABA currents, and may play a role in preventing seizure genesis, and potentially in terminating ongoing seizures (Stell et al., 2003). It is also clear that the contribution of extrasynaptic GABAA receptors changes during maturation, and may contribute to changes in seizure susceptibility during development.
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