Abstract

IntroductionSexual dysfunction is a very important problem in western countries. One of the causes is the treatment with antidepressants; most of the currently available produce sexual dysfunction in men and women (lower libido, anorgasmia, etc.).ObjectiveComparing the nervous system of the animals we expect to find differences to explain the biological substratum of the sexual dysfunction that produce the selective serotonin reuptake inhibitors.MethodTwenty Wistar rats; approximate weight 150 g. It is divided into 4 groups: 2 experimental (paroxetine and agomelatina mouth) and 2 controls. There is a daily conduct. Weighing at the beginning of the study, 14 and 28 days. Is performed sacrifice by decapitation, is extracted from the brain and after fixing paraffin cuts are carried out for their subsequent staining (immunohistochemistry) with their corresponding murine antibody and viewing through optical microscope.ResultsLower immunoreactivity with the antibody anti-TH in the animals treated with paroxetine, at all levels of the dopaminergic activity (tracks mesolimbica, cortical circuit, nigrostriatal pathway and tubero-infundibular). This decrease is reaffirmed after the statistical treatment of data.ConclusionsTreatment with paroxetine in animal models causes a depletion of the dopaminergic system that can be one of the biological bases of sexual dysfunction, altering the reward mechanisms as well as producing hyperprolactinemia.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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