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Nitric oxide (NO) has been thought to be a novel factor involved in the mechanisms of mental disorders pathogenesis for quite some time. However, little is known about potential crosstalk between neuronal NO signaling and neuroleptics action. The present work was, therefore, focused on gene expression of neuronal NO synthase (nNOS) in the brains of rats chronically treated with olanzapine, an atypical antipsychotic drug. Studies were carried out on adult, male Sprague-Dawley rats that were divided into 2 groups: control and experimental animals treated with olanzapine (28-day-long intraperitoneal injection, at dose 5 mg/kg daily). All individuals were killed under anesthesia and the whole brains excised. Immunohistochemical procedure was used for histological assessment of the whole brain, and for both descriptive and quantitative analysis of nNOS protein distribution in selected brain structures. Long-term treatment with olanzapine is reflected in different changes in the number of enzyme-expressing cells in the rat brain. Olanzapine decreased the number of nNOS-expressing cells and possibly reduced NO synthesis in the rat striatum. Olanzapine can be taken into account as a potential inhibitor of NO synthesis in the rat striatum., (© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Austria, part of Springer Nature.)

Neuropeptides are involved in various brain activities being able to control a wide spectrum of higher mental functions. The purpose of this concise structural investigation was to detect the possible immunoreactivity of the novel multifunctional neuropeptide nesfatin-1 within the human bed nucleus of the stria terminalis (BNST). The BNST is involved in the mechanism of fear learning, integration of stress and reward circuits, and pathogenesis of addiction. Nesfatin-1-expressing neurons were identified for the first time in several regions of the BNST using both immunohistochemical and fluorescent methods. This may implicate a potential contribution of this neuropeptide to the BNST-related mechanisms of stress/reward responses in the human brain.