Glutamate is the main excitatory
neurotransmitter in the central nervous system. Dysfunction of the glutamatergic system plays an important and well-established role in the pathogenesis of
schizophrenia. Agents with glutamatergic properties such as
N-methyl-D-aspartate receptor coagonists (ie,
glycine, D-
cycloserine) and
glycine transporter type 1 inhibitors (eg,
sarcosine,
bitopertin) are investigated in
schizophrenia with special focus on negative and cognitive symptomatology. In this article, we describe a case of a 34-year-old woman with diagnosis of
schizophrenia with persistent moderate negative and
cognitive symptoms, a participant of the Polish
Sarcosine Study (
PULSAR) treated with
olanzapine (25 mg per day) and
venlafaxine (75 mg per day). During ten weeks of
sarcosine administration (2 g per day) the patient's activity and mood improved, but in the following 2 weeks, the patient reported decreased need for sleep, elevated mood, libido and general activity. We diagnosed
drug-induced
hypomania and recommended decreasing the daily dose of
venlafaxine to 37.5 mg per day, which resulted in normalization of mood and activity in about 1 week. After this change, activity and mood remained stable and better than before adding
sarcosine, and subsequent depressive symptoms were not noted. We describe here the second case report where
sarcosine induced important affect changes when added to antidepressive and
antipsychotic treatment, which supports the hypothesis of clinically important
glutamate-
serotonin interaction.