2. Adverse effects (FLUOXETINE) Among the common adverse effects associated with fluoxetine and listed in the prescribing information, the effects with the greatest difference from placebo are nausea (22% vs 9% for placebo),insomnia(19% vs 10% for placebo),somnolence(12% vs 5% for placebo),anorexia(10% vs 3% for placebo),anxiety(12% vs 6% for placebo), nervousness (13% vs 8% for placebo),asthenia(11% vs 6% for placebo) and tremor(9% vs 2% for placebo).Those that most often resulted in interruption of the treatment were anxiety, insomnia, and nervousness.
3. Mechanism of action (FLUOXETINE) A serotonin reuptake inhibitor (SRI) is a type of drug that acts as a reuptake inhibitor for the neurotransmitter serotonin (5-hydroxytryptamine (5-HT)) by blocking the action of the serotonin transporter (SERT).This in turn leads to increased extracellular concentrations of serotonin and, therefore, an increase in serotonergic neurotransmission. Fluoxetine's mechanism of action is predominantly that of a serotonin reuptake inhibitor. Fluoxetine delays the reuptake of serotonin, resulting in serotonin persisting longer when it is released. Fluoxetine may also produce some of its effects via its potent 5-HT2C receptor antagonist effects. Fluoxetine affects neurotransmitters, the chemicals that nerves within the brain use to communicate with each other. Neurotransmitters are manufactured and released by nerves and then travel and attach to nearby nerves. Thus, neurotransmitters can be thought of as the communication system of the brain. Serotonin is one neurotransmitter that is released by nerves in the brain. The serotonin either travels across the space between nerves and attaches to receptors on the surface of nearby nerves or it attaches to receptors on the surface of the nerve that produced it, to be taken up by the nerve and released again
4. (SIBUTRAMINE) The serotonin and noradrenaline reuptake inhibitor sibutramine has been licensed as an anti-obesity treatment for more than a decade. However, while inhibitory effects on food intake and weight gain are well documented, surprisingly little published detail exists regarding its influence on feeding and related behaviours. The present study was therefore designed to assess the effects of acute sibutramine treatment on food intake, the behavioural satiety sequence (BSS) and post-treatment weight gain. Subjects were 10 non-deprived adult male Lister hooded rats, tested with 0.5-3.0 mg/kg sibutramine hydrochloride during 1-h DVD-recorded test sessions with palatable mash. Our results show that sibutramine dose-dependently reduced food intake, an effect significant at all doses tested. Ethological analysis revealed very few behavioural effects, except for a dose-dependent reduction in time spent feeding and an increase in the frequency of resting. Behavioural specificity was further supported by time-bin analysis which confirmed both the structural integrity and dose-dependent acceleration of the BSS. Single dosing with sibutramine (3.0 mg/kg) also suppressed daily weight gain over the 24-72 h period post-dosing. Current data support the conclusion that the acute anorectic and weight loss efficacy of sibutramine in adult male rats is not secondary to behavioural disruption but, instead, is due largely to an acceleration in behavioural satiety.
