Moderate til svære depressioner, inkl. forebyggelse af periodisk depression. Panikangst.

Helt ærligt, kunne du ikke have søgt på Google, når nu du har hele navnet?

Men det er antidepressiv, SSRI.

Og så hedder de Citalopram.

Jamen hvad er virkningen på "normale" mennesker, der ikke har brudg for dem?

Jeg er heller ikke interesseret i at få "lammepiller".. Tager aldrig piller, medmindre jeg gerne vil sove ovenpå en tur, på stimulanser. men det er ikke for at lamme mig selv, men for at sove.
Så man kan heller ikke bruge disse piller til sovepiller?

De kan muligvis bruges efter en tur på MDMA, ligesom 5 htp bliver brugt. Men ellers er der intet sjovt ved dem

what the fuck? Hvordan har du fået det ind i hovedet?

Så vidt jeg ved bruges SSRI'er til at genopbygge bla. ens sertonins center. og at blande mdma med ssri er NO GO. så læs på lektien før du kommer med sindsyge råd.

Så vidt jeg ved bruges SSRI'er til at genopbygge bla. ens sertonins center. og at blande mdma med ssri er NO GO. så læs på lektien før du kommer med sindsyge råd.

Så vidt jeg ved bruges SSRI'er til at genopbygge bla. ens sertonins center. og at blande mdma med ssri er NO GO. så læs på lektien før du kommer med sindsyge råd.

The time course of damaging events in rats can be seen by administering SSRIs, such as fluoxetine and citalopram, after MDMA. Pretreatment with fluoxetine (Prozac) or citalopram (Celexa) has been shown to block the neurotoxicity of MDMA (Battaglia, 1988; Schmidt 1987; 1990; Shankaran, 1999a), probably by blocking interactions of MDMA with SERT. More interestingly, fluoxetine remains almost fully protective if given 3 or 4 hours after MDMA. By 4 hours, most of the MDMA-induced release of 5-HT and DA has already occurred (Gough, 1991; Hiramatsu, 1990) and increases in extracellular free radicals (Colado, 1997b; Shankaran, 1999a) and lipid peroxidation (the alteration of fat molecules by free radicals) (Colado, 1997a) can be measured. Nevertheless, the administration of fluoxetine at this point decreases subsequent extracellular oxidative stress (Shankaran, 1999a) and long-term 5-HT depletions (Schmidt, 1987; Shankaran, 1999a). Fluoxetine will still be partially protective if given 6 hours after MDMA but has no protective effect 12 hours after administration (Schmidt, 1987). This shows that neurotoxic MDMA regimens initiate a series of events that become increasingly damaging between 3 and 12 hours after drug administration in rats.

Slow recovery of serotonergic functioning can be seen following a neurotoxic dose of MDMA. The extent of recovery is different in different species. In rats, there is extensive recovery of indicators of serotonergic functioning 1 year after drug exposure (Battaglia, 1988; Lew, 1996; Sabol, 1996; Scanzello, 1993), although there is significant variation in recovery between individual animals (Fischer, 1995). In primates, some recovery of serotonergic function occurs but is less extensive than in the rat. Altered serotonergic axon density was still detectable 7 years after MDMA exposure in one study of squirrel monkeys (Hatzidimitriou, 1999). Therefore, despite some recovery, MDMA-induced serotonergic changes are likely permanent in this primate species. This apparent species difference may be partially related to the more severe initial serotonergic damage usually seen in primates compared to rats, but also likely indicates a species difference in regrowth of serotonergic axons.