Although the basal GABA release in hippocampus and amygdala and the global SV2A expression level in inhibitory neurons remained unaffected, the authors observed reduced activity-induced GABAergic (but not glutamatergic) release and higher susceptibility of the animals to kindling-induced epileptogenesis, again suggesting the complicated relationship between SV2A and GABAergic transmission in epilepsy. Here, SV2A is linked to epilepsy.