Cysteamine Potentiates the Anti-Depressive Effects of Venlafaxine in Corticosterone-Induced Anxiety/Depression Mouse Model: Effect on Brain-Derived Neurotrophic Factor and Tropomyosin-Related Kinase B

Ahmed, Eman;Tawfik, Mona K.;Essawy, Soha S.;Ahmed, Amal S.;Hermans, Emmanuel
(2018) Egyptian Journal of Basic and Clinical Pharmacology — Vol. 8 (2018)

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Authors
  • Ahmed, Eman
    Author
  • Tawfik, Mona K.
    Author
  • Essawy, Soha S.
    Author
  • Ahmed, Amal S.
    Author
  • Author
Abstract
The hypothalamic-pituitary-adrenal (HPA) axis abnormalities have been linked to the occurrence of severe depressive and anxiety states. Venlafaxine, a serotonin and a noradrenaline reuptake inhibitor (SNRI), is an approved antidepressant agent with evidence of non-response to treatment in a subset of patients. In this study, 48 male mice (30-38 g) were used to evaluate the possible anxiolytic and antidepressant influence of intraperitoneal (i.p.) cysteamine (150 mg/kg/day) on i.p. venlafaxine (10mg/Kg and 20mg/Kg), as well as effects on brain-derived neurotrophic factor (BDNF) level and tropomyosin-related kinase B (TrkB) gene expression in prefrontal cortex (PFC) in corticosterone-induced anxiety/depression mouse model. The present results provided evidence on insufficient venlafaxine anxiolytic and antidepressant effects in this model. However, cysteamine combined with venlafaxine caused significant antidepressant behavioral effects together with a significant increase in BDNF levels followed by TrkB receptor downregulation in mice PFC. In conclusion, we highlight the potential use of a combination therapy of venlafaxine and cysteamine as a therapeutic strategy for glucocorticoid-related symptoms of depression.
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Ahmed, E., Tawfik, M. K., Essawy, S. S., Ahmed, A. S., & Hermans, E. (2018). Cysteamine Potentiates the Anti-Depressive Effects of Venlafaxine in Corticosterone-Induced Anxiety/Depression Mouse Model: Effect on Brain-Derived Neurotrophic Factor and Tropomyosin-Related Kinase B. Egyptian Journal of Basic and Clinical Pharmacology, 8. https://doi.org/10.11131/2018/101383 (Original work published 2018)