The effect of finasteride on anxiety in rats

Introduction: The traditional neurobiological concept of the etiology of anxiety disorders is based on the monoamine hypothesis, which suggests that mood disorders are caused by a deficiency in serotonin or noradrenaline transmission at functionally important receptors in the brain. Recent studies have provided strong evidence that gamma-aminobutyric acid (GABA) is involved in the pathophysiology of the anxiety as well. By blocking 5α-reductase in the brain, finasteride (FIN) inhibits the synthesis of allopregnanolone (ALLO) and tetrahydrodeoxy-corticosterone (THDOC) in a dose-dependent manner and redirects progesterone to alternative metabolic pathways, the effects that change GABAergic transmission and affect the emotional state. Aim: The aim of this study was to investigate the effect of finasteride as GABAergic transmission modulator, on anxiety in rats. Materials and methods: Male Wistar rats were divided into the groups: 1. control treated with 2-hydroxypropyl-β-cyclodextrin; 2. finasteride-treated, FIN (150 mg/kg). Daily doses of FIN (50 mg/kg) were administered intraperitoneally during three days. The level of anxiety was measured 24 hours after the administration of the last dose of FIN using elevated plus maze and light-dark test. Results: In the elevated plus maze, the total time spent in the open arms was not significantly different in FIN compared to control group (p u003e 0.05). In addition, there was no significant difference in the number of crossings from one arm to the other via the central platform in FIN vs. control group (p u003e 0.05). In the light-dark test, the time that animals, from FIN group spent in the light part of the box, was significantly lower compared to the same parameter recorded in animals from the control group (p u003c 0.05). Conclusion: Finasteride exerts anxiogenic effects in rats, dominantly causing bright space anxiety-like behavior. Finasteride has no significant effect on the open space anxiety-like behavior.