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Re: Acamprosate Calcium/SLS » Anna P.

Posted by SLS on June 2, 2002, at 9:58:59

In reply to Re: Acamprosate Calcium/SLS, posted by Anna P. on June 1, 2002, at 23:55:20

Hi Anna.


> Are you shure they use Memantine in Germany for depression as well?

I think I was wrong about the extent to which memantine is used to treat depression. I probably exaggerated in my mind some of the stuff I bumped into on the Internet. I included two abstracts to be found below.

> I'm just wondering if they have energizing or sedating effect.

I'm not sure. One thing I read stated that acamprosate was neither sedating nor produced euphoria.

> Are you ready to try either Acamprosate or Memantine?

I don't know what I'm doing right now. Things are progressing too slowly for me. I think my doctor might be treating me too conservatively, as he likes to manipulate only one drug at a time and ask that I wait 3-4 weeks before deciding on what to do next. This is probably the right way to treat the average case, but perhaps it makes sense for me to throw as much sh_t against the wall as possible in the hope that some of it will stick.

For some reason, I am inept at advocating for myself. I tend to be a people-pleaser and yield to authority. I think depression leaves me too passive and indecisive and without the focus and energy to make things happen. I have never taken it upon myself to get a hold of drugs and play with them. I see people here go through so many drugs and dosage changes. I'm not sure if most of these people are doing this without the consent or knowledge of their doctors or what. Have I been missing the boat? Right now, I am content to remain with my current doctor through my next trial of Nardil. I should really see someone else for a consultation, though. I'm thinking of seeing Ivan Goldberg, MD.

> I'm interested in trying Acamprosate for my cyclothymia, treatment-resistant depression and poop-out of the medications. I had a miracle response for the combination of Moclobemide and Revia (Naltrexone) that lasted for about six months, than faded.

Ain't it something... how different the whole world is when you respond to medication. I experienced a six-month remission in 1997. Gosh, it was like living a whole other life.

Are you still taking Revia? Moclobemide is notorious for pooping-out. Have you tried to substitute for it using another MAOI?


- Scott


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: Neuropharmacology 1999 Jun;38(6):735-67 Related Articles, Books, LinkOut


Memantine is a clinically well tolerated N-methyl-D-aspartate (NMDA) receptor antagonist--a review of preclinical data.

Parsons CG, Danysz W, Quack G.

Department of Pharmacological Research, Merz and Co., Frankfurt am Main, Germany. chris.parsons@merz.de

N-methyl-D-aspartate (NMDA) receptor antagonists have therapeutic potential in numerous CNS disorders ranging from acute neurodegeneration (e.g. stroke and trauma), chronic neurodegeneration (e.g. Parkinson's disease, Alzheimer's disease, Huntington's disease, ALS) to symptomatic treatment (e.g. epilepsy, Parkinson's disease, drug dependence, depression, anxiety and chronic pain). However, many NMDA receptor antagonists also produce highly undesirable side effects at doses within their putative therapeutic range. This has unfortunately led to the conclusion that NMDA receptor antagonism is not a valid therapeutic approach. However, memantine is clearly an uncompetitive NMDA receptor antagonist at therapeutic concentrations achieved in the treatment of dementia and is essentially devoid of such side effects at doses within the therapeutic range. This has been attributed to memantine's moderate potency and associated rapid, strongly voltage-dependent blocking kinetics. The aim of this review is to summarise preclinical data on memantine supporting its mechanism of action and promising profile in animal models of chronic neurodegenerative diseases. The ultimate purpose is to provide evidence that it is indeed possible to develop clinically well tolerated NMDA receptor antagonists, a fact reflected in the recent interest of several pharmaceutical companies in developing compounds with similar properties to memantine.

Publication Types:
Review
Review, Academic

PMID: 10465680 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10465680&dopt=Abstract


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Antidepressant drugs inhibit glucocorticoid receptor-mediated gene transcription - a possible mechanism.

Budziszewska B, Jaworska-Feil L, Kajta M, Lason W.

Department of Endocrinology, Institute of Pharmacology, Polish Academy of Sciences, Krakow, Poland.

1. Antidepressant drugs are known to inhibit some changes evoked by glucocorticoids, as well as a hyperactivity of hypothalamic-pituitary-adrenal (HPA) axis, often observed in depression. 2. The aim of present study was to investigate effects of various antidepressant drugs on the glucocorticoid-mediated gene transcription in fibroblast cells, stably transfected with an MMTV promoter (LMCAT cells). 3. The present study have shown that antidepressants (imipramine, amitriptyline, desipramine, fluoxetine, tianeptine, mianserin and moclobemide), but not cocaine, inhibit the corticosterone-induced gene transcription in a concentration- and a time-dependent manner. 4. Drugs which are known to augment clinical effects of medication in depressed patients (lithium chloride, amantadine, memantine), do not affect the inhibitory effects of imipramine on the glucocorticoid receptor (GR)-mediated gene transcription. 5. Inhibitors of phospholipase C (PLC), protein kinase C (PKC), Ca(2+)/calmodulin-dependent protein kinase (CaMK) and antagonists of the L-type Ca(2+) channel also inhibit the corticosterone-induced gene transcription. 6. Inhibitors of protein kinase A (PKA) and protein kinase G (PKG) are without effect on the GR-induced gene transcription. 7. Phorbol ester (an activator of PKC) attenuates the inhibitory effect of imipramine on the GR-induced gene transcription. 8. Imipramine decreases binding of corticosterone-receptor complex to DNA. 9. It is concluded that antidepressant drugs inhibit the corticosterone-induced gene transcription, and that the inhibitory effect of imipramine depends partly on the PLC/PKC pathway.

PMID: 10903980 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10903980&dopt=Abstract


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