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.

一氧化氮（NO）长期以来被认为是参与精神障碍发病机制的一种新因素。然而，人们对神经元 NO 信号传导与精神安定药作用之间潜在的串扰知之甚少。因此，目前的工作重点是长期接受非典型抗精神病药物奥氮平治疗的大鼠大脑中神经元一氧化氮合酶（nNOS）的基因表达。研究对象是成年雄性 Sprague-Dawley 大鼠，分为 2 组：对照组和用奥氮平治疗的实验动物（腹腔注射 28 天，剂量为每天 5 mg/kg）。所有个体均在麻醉下被杀死并切除整个大脑。免疫组织化学程序用于全脑的组织学评估，以及对选定脑结构中 nNOS 蛋白分布的描述性和定量分析。奥氮平长期治疗反映在大鼠脑内酶表达细胞数量的不同变化。奥氮平减少了表达 nNOS 的细胞数量，并可能减少了大鼠纹状体中 NO 的合成。奥氮平可被认为是大鼠纹状体中 NO 合成的潜在抑制剂。