Abstract
Fluoxetine serves as a primary drug for the pharmacological treatment of binge eating. Its activity usually consists in blocking 2C serotonin receptors. This may be considered to be controversial since agonists of this receptor are effective in pharmacological treatment of bulimia. Bulimia episodes occur as a result of a decrease in serotonergic activity in the central nervous system. The mechanism is clinically confirmed. Drugs which increase the activity of the serotonin system in suppressing binge eating proved effective. The anorexigenic effect of drugs which increase the activity of the serotonin system results from the stimulation of serotonin receptors and not from their blocking. Appetite regulation and binge eating are associated with the activity of the dopaminergic and serotonergic systems. Experimental studies conducted so far prove that the increase in dopaminergic activity in the structures of the reward system is caused by stimulation, and not blocking, of serotonin 2C receptors. The anorexigenic effect of proserotonin drugs may also result from the stimulation of type 3 serotonin receptors and possibly 2C on neurons located in the nucleus of solitary tract. The psychopharmacological investigation conducted in this paper revealed the role of 5-HT2C receptors in the pathogenesis of bulimia nervosa and the mechanism of action of fluoxetine in the treatment of binge eating. Based on existing knowledge, the fact that fluoxetine blocks these receptors does not appear to play a significant role in appetite suppression. Due to few experimental works, the problem requires further research.