Tryptophan hydroxylase (TPH) is crucial for serotonin production, and TPH2 is primarily expressed in neurons. Human TPH2 variants are associated with major depressive, bipolar, and attention-deficit/hyperactivity disorders. Tph2 knockout (KO) in mice increases impulsivity and aggression. An imbalance in several transmitter systems, including serotoninergic signalling, also influences the process of medial prefrontal cortex (mPFC) development. The BALB/cJ mouse model with low serotonin shows altered distribution of Parvalbumin-positive (PV+) interneurons in the anterior cingulate (ACC) and midcingulate cortices (MCC). We anticipate that a) Tph2 KO in mice reduces the amount of PV+-interneurons, resulting in frontostriatal circuitry dysfunction and increased impulsivity/aggression, and that b) optogenetic manipulation of PV+ interneurons may modulate impulsivity/aggression. To validate this hypothesis, the following methods will be used: a) Immunofluorescence labelling of PV+ cells across ACC and MCC slices, b) Western blot and gene expression analysis for effects caused by altered PV+ cell subpopulation distribution, and c) optogenetic manipulation of PV+-interneurons in ACC to modulate cell activity and reduce impulsivity/aggression. Preliminary data showed that there were no significant differences in the distribution of PV+-interneurons in male animals. Nevertheless, female knockout animals show a significant reduction in PV+-interneuron density in both ACC and MCC compared to heterozygous and wildtype animals. A reduced amount of PV+-interneurons may affect frontostriatal circuitry, contributing to impulsive and aggressive behaviors in KO mice. The objective of the forthcoming experiments is to validate the initial findings and explore potential mechanisms underlying strong differences observed in female mice when compared to males.