people suffer from epilepsy, and 30% of them do not respond with traditional antiepileptic drugs. Thus, different strategies for seizures control in such patients are required. Seizures are the result of an imbalance between excitatory and inhibitory impulses on the central nervous system, being glutamate (GLU) the major excitatory neurotransmitter. GLU participates in several physiological but also pathological processes, including epilepsy. For recycling, to avoid neurotoxicity of ammonium generated during its metabolism and to finish its excitatory effect as neurotransmitter, GLU is removed from the synaptic cleft to the glia and back to neurons by GLU transporters, a family of proteins called EAATs. In neurons EAAT3 is highly expressed, which dysfunction has been implicated in epilepsy. EAATs activity is regulated by external GLU levels, and coupling GLU transportation by EAATs with the activity of enzymes related to its metabolism would improve the efficiency of the process. Here we study EAAT3 as a mechanism to counteract glutamatergic overstimulation that occurs in seizures.
Audience take away:
• Clarify a little bit more the roll of EAAT3 in seizures mechanism.
• To explore the coupling of GLU transportation through EAAT3 with its oxidative deamination.
• Study the possibility of controlling seizures through modulations of EAAT3 activity.
• Evaluate the possibility of EAAT3 as a pharmacological target for the development of new antiepileptic drugs.