ADORA2A and epilepsy: This is in accordance with the established role of A2AR in the control of NMDA receptors and synaptic plasticity processes, rather than to control excitability, which is a function instead fulfilled by A1R (for review, see Cunha, 2016), This prompts A2AR antagonists as novel “secondary neuroprotective agents” (Meldrum, 2002) arresting the limbic maladaptive plasticity underlying the progressive severity of epilepsy (Meldrum, 2002; Pitkänen and Sutula, 2002; Löscher and Brandt, 2010).