Short ReportGlucocorticoid and brain-derived neurotrophic factor relationship a brief investigation into the model of depression by chronic administration of corticosteronePereira, Gabriele C.; Roversi, Karine; Trevisan, Gabriela; Burger, Marilise E.; Bochi, Guilherme V.Author Information Programa de Pós-Graduação em Farmacologia, Universidade Federal de Santa Maria (UFSM), Santa Maria (RS), Brazil Received 4 October 2019 Accepted as revised 30 December 2019 Correspondence to Guilherme V. Bochi, PhD, Departamento de Fisiologia e Farmacologia, Centro de Ciências da Saúde, Universidade Federal de Santa Maria, Avenida Roraima 1000, Prédio 21, Sala 5117, Camobi, 97105-900 Santa Maria (RS), Brazil, E-mail: firstname.lastname@example.org Behavioural Pharmacology: June 2020 - Volume 31 - Issue 4 - p 407-412 doi: 10.1097/FBP.0000000000000547 Buy Metrics Abstract Depression is considered a common mental disorder that affects more than 300 million people worldwide. Despite this high incidence, its etiology is not completely elucidated instigating further studies. For this purpose, different animal models are used to study routes and molecular changes involved in depression, among them the chronic administration of corticosterone. However, the knowledge about neurochemical changes after this protocol is still controversial. In this work, we evaluated serum corticosterone levels, adrenal/body weight ratio, as well as glucocorticoid receptor and brain-derived neurotrophic factor protein expression and its receptor, tropomyosin-receptor kinase B. These analyzes were performed on prefrontal cortex, hippocampus, and striatum samples taken of mice after 21 days of administration of corticosterone. Exposure to corticosterone reduced the serum corticosterone levels and the adrenal/body weight ratio. Moreover, the glucocorticoid receptor and tyrosine-receptor kinase B expression were increased in the hippocampus while the brain-derived neurotrophic factor expression was reduced in the prefrontal cortex. We also found a positive correlation between the expression of glucocorticoid receptor and tyrosine-receptor kinase B and our results suggest a possible relationship between the glucocorticoid/glucocorticoid receptor and brain-derived neurotrophic factor/tropomyosin-receptor kinase B routes after chronic corticosterone administration. To our knowledge, this is the first study that evaluate these parameters concomitantly in important mood-related structures. In addition, these results may be useful to other research groups seeking to explore new pathways and substances with therapeutic potential to treat this silent epidemic. Copyright © 2020 YEAR Wolters Kluwer Health, Inc. All rights reserved.