Preclinical studies have also shown other mechanisms of riluzole that potentially impact glutamatergic dysfunction in schizophrenia: (i) increase in the astrocytic reuptake of glutamate [228]; (ii) neuroprotective effect via the upregulation of glutamate transporter 1 (GLT-1) in a voltage-sensitive ion channels blockade independent manner [229]; (iii) improved cortical glutamate cycling [230]; and (iv) reducing the size of the releasable presynaptic glutamate, inhibiting protein kinase C (PKC)-dependent Munc18-1 phosphorylation [231] (Figure 3). This evidence concerns the gene PRRT2 and schizophrenia.