In this view, our previous study [29] has shown that 4 days of α-T treatment after kainate-induced SE is able to (1) quench neurodegenerative and neuroinflammatory processes triggered by SE; (2) counteract glutamine synthase decline, recovering the glutamate–glutamine–GABA cycle pathway, which has been found to be disrupted in the hippocampus of patients affected by temporal lobe epilepsy (TLE) [62]; (3) induce an increase in dendritic spine number and in synaptophysin immunoreactivity, suggesting a role of α-T in synaptogenesis promotion and/or synapse protection. Here, GLUL is linked to temporal lobe epilepsy.