In this study, the authors investigated the effects of chronic administration of aripiprazole and NAC on schizophrenia-like behaviors and anaerobic cysteine metabolism in the hippocampus. The schizophrenia-type changes were induced in SD rats by repeated administration the glutathione synthesis inhibitor L-butionine-(S,R)-sulfoximine in combination with the dopamine reuptake inhibitor GBR 12909 in the early postnatal period. In the hippocampus, the level of anaerobic cysteine metabolites, H2S and bound sulfane sulfur, were determined by a fluorescence method, while the expression of H2S-synthetizing enzymes: CBS and MST by Western blot. Chronic treatment with aripiprazole or NAC reversed social and cognitive deficits and reduced the exploratory behaviors. In the hippocampus of 16-day-old model pups, H2S levels and MST protein expression were significantly decreased. In adult model rats, H2S levels remained unchanged, bound sulfane sulfur significantly increased, and the expression of CBS and MST slightly decreased. The studied drugs significantly reduced the level of bound sulfane sulfur and the expression of tested enzymes. The reduction in bound sulfane sulfur level coincided with the attenuation of exploratory behavior. The data of this study are interesting. This article is well written. However, the following minor concerns should be addressed.

1) Please include the schedule of treatments, behavioral tests, and sample collection in the Figure 1A.

2) In this study, the authors measured levels of monoamines. However, the authors stated the role of NMDAR in mechanisms of action of H2S in the introduction and discussion sections. Did you measure levels of NMDAR-related amino acids (e.g., glutamate, glutamine, L-serine, D-serine, glycine, GABA) in the same brain regions? Please state this in the limitation section.

3) Methods: Please include the catalog number of antibodies used in this study.