Glutamate is the main excitatory neurotransmitter of the brain. Dysfunctional glutamatergic transmission leads to important neuropsychiatric consequences playing a primary role in the pathogenesis of numerous disorders, such as schizophrenia, addictions, or Alzheimer’s dementia.1–5 Currently investigated possibilities of pharmacological intervention in schizophrenia are focused on enhancing the N-methyl-D-aspartate (NMDA) receptor activity according to the hypo-NMDA receptor hypothesis of that psychosis. NMDA receptor is one of the glutamatergic ionotropic receptors of crucial importance for cognition (eg, attention and memory dependent on long-term potentiation process) which is probably also related to negative symptoms present in schizophrenia.6–8 In literature, there are two pharmacological opportunities described for enhancing function of the NMDA receptor. The direct method relies on administration of glycine (natural coagonist of the NMDA receptor) or other coagonists (D-cycloserine and D-serine), and the indirect method relies on inhibiting the glycine transporter type I (GlyT-1) with sarcosine, bitopertin (RG1678), or ALX-5407.9–12 Sarcosine (N-methylglycine) has been used in several small studies and the results seem to be promising in ameliorating cognitive and negative symptoms where efficacy of using known antipsychotics is rather limited.13,14 Previously
