{"title":"The effect of nicotine on antidepressant and anxiolytic responses induced by citalopram and citicoline in mice.","authors":"Fatemeh Khakpai, Mohammad-Reza Zarrindast","doi":"10.55782/ane-2023-017","DOIUrl":null,"url":null,"abstract":"<p><p>The effect of nicotine on both anxiety and depression has been broadly studied. Moreover, citalopram and citicoline play a role in the modulation of anxiety and depression. This study was designed to examine the effects of nicotine on the antidepressant and anxiolytic responses induced by citalopram and citicoline in mice. Anxiety‑ and depression‑related behaviors were assessed with the elevated plus maze and forced swim test, respectively. The results showed that subcutaneous administration of nicotine decreased open‑arm time (OAT) and open‑arm entries (OAE) but increased immobility time, suggesting anxiogenic‑like and depressive‑like effects. Intraperitoneal administration of citalopram increased OAT but decreased immobility time, indicating that citalopram induced anxiolytic‑like and antidepressant‑like responses. Additionally, an injection of citicoline increased OAE but decreased immobility time, revealing anxiolytic‑like and antidepressant‑like effects. Interestingly, the subthreshold dose of nicotine potentiated the citalopram and citicoline effects on OAT and immobility time, which revealed anxiolytic‑like and antidepressant‑like behaviors. Locomotor activity was not significantly changed by any doses of the drugs. In conclusion, these findings suggest that interactions between nicotine and citalopram or citicoline occur upon induction of anxiolytic and antidepressant responses in mice.</p>","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"83 2","pages":"194-202"},"PeriodicalIF":1.4000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Acta neurobiologiae experimentalis","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.55782/ane-2023-017","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NEUROSCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
The effect of nicotine on both anxiety and depression has been broadly studied. Moreover, citalopram and citicoline play a role in the modulation of anxiety and depression. This study was designed to examine the effects of nicotine on the antidepressant and anxiolytic responses induced by citalopram and citicoline in mice. Anxiety‑ and depression‑related behaviors were assessed with the elevated plus maze and forced swim test, respectively. The results showed that subcutaneous administration of nicotine decreased open‑arm time (OAT) and open‑arm entries (OAE) but increased immobility time, suggesting anxiogenic‑like and depressive‑like effects. Intraperitoneal administration of citalopram increased OAT but decreased immobility time, indicating that citalopram induced anxiolytic‑like and antidepressant‑like responses. Additionally, an injection of citicoline increased OAE but decreased immobility time, revealing anxiolytic‑like and antidepressant‑like effects. Interestingly, the subthreshold dose of nicotine potentiated the citalopram and citicoline effects on OAT and immobility time, which revealed anxiolytic‑like and antidepressant‑like behaviors. Locomotor activity was not significantly changed by any doses of the drugs. In conclusion, these findings suggest that interactions between nicotine and citalopram or citicoline occur upon induction of anxiolytic and antidepressant responses in mice.
期刊介绍:
Acta Neurobiologiae Experimentalis (ISSN: 0065-1400 (print), eISSN: 1689-0035) covers all aspects of neuroscience, from molecular and cellular neurobiology of the nervous system, through cellular and systems electrophysiology, brain imaging, functional and comparative neuroanatomy, development and evolution of the nervous system, behavior and neuropsychology to brain aging and pathology, including neuroinformatics and modeling.