Male sexual function has been a topic of high interest for the scientific community for the last decades. Approximately 20 to 30% of the male population suffers from some kind of sexual dysfunction that although it might not be life threatening, it can significantly affect emotionally and interpersonally the relationships of inflicted men. Its origins are motive of controversy as they can be a result of several psychosocial, biological and genetic factors that may emotionally condition a person to have elevated anxiety levels before or during the sexual encounter, resulting in unsuccessful performance. Some of the most prevalent dysfunctions are premature and delayed ejaculation (PE-DE). Even though drugs like selective serotonin transporter inhibitors (SSRIs) are used as treatment for PE, a large number of men relapses as chronic use of these drugs in the long run may adversely affect ejaculatory and sexual behavior, causing chronic SSRI sexual dysfunction. On this work we investigated further mechanisms involved in the expression of ejaculatory sexual dysfunctions. We correlated a different brain structure to the execution of the sexual function, further studied the role of the serotonin transporter in sexual performance by using the SERT knockout rat and set it as a genetic animal model that resembles chronic SSRI induced sexual dysfunction in humans, found that tramadol has an “on-demand” effect in SERT+/+(normal), SERT+/- and SERT-/- rats mainly due to its SSRI component, and shown that pre and post-synaptic 5-HT1A receptor biased agonists have a prosexual effect in the expression of sexual function.
|Qualification||Doctor of Philosophy|
|Place of Publication||[Groningen]|
|Publication status||Published - 2019|