Anxiety and depression are among the major neuropsychiatric disorders worldwide, and yet the etiologies of these disorders remain unclear to date. Chronic unpredictable stress (CUS) procedure mimics several behavioral characteristics such as anxiety and depression in rodents. Using this animal model, we have attempted to understand the serotonergic system in the hippocampus and prefrontal cortex, while using the 5-HT_2CR agonist and antagonist in evaluating 5-HT_2C receptor neurotransmission. A decrease in serotonin (5-HT) level, tryptophan hydroxylase-2 activity and, 5-HT_2CR receptor protein down-regulation in the CUS exposed group, explains the involvement of 5-HT and 5-HT_2CR neurotransmission in the genesis of anxiety and depression. Besides, the oxidative stress - attenuated electrolyte imbalance via decrease ATPase pump activity, and compromised oxidative phosphorylation via decrease ETC-I activity are some of the underlying factors affecting neuronal cell survival and serotonergic neurotransmission. To complement our finding, altered behavioral performance scored in the open field test, elevated plus maze test, and the forced swim test, when exposed to CUS is indicative or consistent with anxiety, depression, emotional and locomotor status of the animals. Keeping these findings in mind, treatment with 5-HT_2CR agonist (1-Methylpsilocin at 0.7 mg/kg), and 5-HT_2CR antagonist (RS-102221 hydrochloride at 1 mg/kg) displayed varying results. One prominent finding was the anxiolytic ability of the 5-HT_2CR agonist and the anti-depressive ability of the 5-HT_2CR antagonist on the 7th-day treatment. Though the exact mechanism of action is not clear, their ability to equilibrate brain redox status, restoring Ca²⁺ level via Ca²⁺ATPase pump activity, and sustaining the mitochondrial bioenergetics can all be accounted for facilitating neurogenesis and the serotonergic system.

焦虑和抑郁是世界范围内主要的神经精神疾病，但迄今为止，这些疾病的病因尚不清楚。慢性不可预测压力 (CUS) 程序模拟了啮齿类动物的几种行为特征，例如焦虑和抑郁。使用该动物模型，我们尝试了解海马和前额叶皮层中的血清素能系统，同时使用 5-HT _2C R 激动剂和拮抗剂评估 5-HT _2C受体神经传递。CUS 暴露组中血清素 (5-HT) 水平、色氨酸羟化酶-2 活性和 5-HT _2C R 受体蛋白下调的降低解释了 5-HT 和 5-HT _{2C 的参与}R 神经传递在焦虑和抑郁的起源中。此外，氧化应激——通过降低 ATPase 泵活性减弱电解质失衡，以及通过降低 ETC-I 活性破坏氧化磷酸化是影响神经元细胞存活和血清素能神经传递的一些潜在因素。为了补充我们的发现，当暴露于 CUS 时，在露天试验、高架十字迷宫试验和强迫游泳试验中得分的改变的行为表现表明或符合动物的焦虑、抑郁、情绪和运动状态。牢记这些发现，用 5-HT _2C R 激动剂（0.7 mg/kg 的 1-甲基psilocin）和 5-HT _{2C 治疗}R 拮抗剂（1 mg/kg 的 RS-102221 盐酸盐）显示出不同的结果。一个突出的发现是5-HT的能力抗焦虑_2C R激动剂和5-HT的抗抑郁能力_2C - [R拮抗剂第7天的治疗。尽管确切的作用机制尚不清楚，但它们平衡大脑氧化还原状态、通过 Ca ²⁺ ATPase 泵活性恢复 Ca ²⁺水平和维持线粒体生物能量的能力都可以解释为促进神经发生和血清素能系统。