The purpose of our research is to better understand the possible role(s) of this protein through the phenotype of cKO (Grik4 Cre+/-, SV2A lox/lox) mice, male and female, which present a specific decrease of SV2A expression levels in the hippocampal glutamatergic neurons but without any epileptic seizures.
The SV2A isoform is the most studied and its implication in epilepsy therapy led to the development of the first SV2A PET radiotracer [<sup>18</sup>F]UCB-H.
Synaptic vesicle protein 2A (SV2A), which plays an important role in the pathophysiology of epilepsy, is a unique vesicular protein recognized as a pharmacological target of anticonvulsant drugs.
Furthermore, these SV2A modifications may depend on specific changes in the nerve tissue following the induction of epilepsy and might be present in both excitatory and inhibitory terminals.
In addition, a recent clinical study demonstrated that a missense mutation in the SV2A gene caused intractable epilepsy with involuntary movements and developmental retardation, illustrating a causative role of SV2A dysfunction in epilepsy.
To correlate SV2A expression in surgically removed tumor and peritumoral tissue of glioma patients with epilepsy with the clinical response to levetiracetam in a prospective cohort.
Finally, there is a strong correlation between the affinity of a compound for SV2A and its ability to protect against seizures in an audiogenic mouse animal model of epilepsy.