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Re: Sibutramine (Meridia) - Starting it tomorrow.

Posted by SLS on August 4, 2006, at 17:52:24

In reply to Re: Sibutramine (Meridia) - Starting it tomorrow. » SLS, posted by theo on August 4, 2006, at 16:04:36

> Isn't Meridia an obesity drug?

Yup.

It was originally developed as an antidepressant.

Sibutramine and its metabolites are reuptake inhibitors of serotonin, norepinephrine, and dopamine. During clinical trials for depression, I guess weight-loss showed up as a predominant side effect, and the rest was history...

The clinical trials of sibutramine for depression do not appear on Medline. They are probably too old. I guess one would have to leave cyberspace temporarily and travel to an actual library to search out real medical journals. However, one could review the studies involving binge-eating and note the effect sibutramine has on mood in that disorder.

Back in the old days, I don't particularly care how well sibutramine performed compared to placebo or imipramine. All it has to do now is perform well for me. N=1

Interestingly, sibutramine was the only antidepressant tested that rapidly downregulated NE alpha-2 presynaptic autoreceptors.


1: Psychopharmacology (Berl). 1992;107(4):497-502.

A comparison of various antidepressant drugs demonstrates rapid desensitisation of alpha 2-adrenoceptors exclusively by sibutramine hydrochloride.

Heal DJ, Prow MR, Gosden J, Luscombe GP, Buckett WR.

Boots Pharmaceuticals Research Department, Nottingham, UK.

The functional status of presynaptic and postsynaptic alpha 2-adrenoceptors in murine brain was respectively monitored using the hypoactivity (sedation) and mydriasis (pupil dilatation) responses to clonidine (0.1 mg/kg IP). Both responses were attenuated 24 h after 3 days of injection of sibutramine hydrochloride (3 mg/kg IP). To ascertain whether this property was exclusive to sibutramine, the following antidepressant drugs were also tested for their ability to down-regulate alpha 2-adrenoceptors rapidly: amitriptyline, doxepin, nomifensine, desipramine, amoxapine, fluoxetine, zimeldine, tranylcypromine and mianserin. When given for 3 or 5 days at the low dose of 3 mg/kg IP, none of the other antidepressants reduced clonidine-induced hypoactivity or mydriasis. Furthermore, increasing the dose of amitriptyline, doxepin, nomifensine, desipramine, amoxapine and tranylcypromine to 10 mg/kg IP did not enable these antidepressants to attenuate the alpha 2-adrenoceptor-mediated responses after 3 days of treatment. An electroconvulsive shock (ECS; 200 V, 2 s) given once daily attenuated clonidine-induced mydriasis, but not hypoactivity, when administered for 3 days and both responses when administered for 5 days. In conclusion, this comparative study using antidepressant treatments with differing pharmacological modes of action demonstrated that sibutramine was the only drug which rapidly down-regulated pre- and postsynaptic alpha 2-adrenoceptors. ECS down-regulated postsynaptic alpha 2-adrenoceptors when given for 3 days, but required 5 days to desensitise both alpha 2-adrenoceptor populations.

PMID: 1351304 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1351304&dopt=Abstract


- Scott

 

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