Psycho-Babble Medication | about biological treatments | Framed
This thread | Show all | Post follow-up | Start new thread | List of forums | Search | FAQ

Clearing confusion about low/high dose amisulpride

Posted by scott-d-o on January 13, 2004, at 16:37:34

In reply to Re: Amisulpride, posted by falconman on January 12, 2004, at 14:02:52

> > For me, Amisulpride only worked at lower doses. I took it at 25mg. Anything above 50 for me was counterproductive.
>
> What specifically do you mean by counterproductive- What effects did you get off 100mg?
> Thanks

I can't speak for the above poster, however, the reason amisulpride may only be effective at very low doses is due to the type of receptors it binds to. The two different types we are concerned with are presynaptic (also called autoreceptors) and postsynaptic. When dopamine binds to a postsynaptic receptor, it transmits the nerve impulse to the receiving cell. However, autoreceptors are located on the dopamine-producing cells themselves and help the cell gauge how much dopamine to release into the synaptic space (so when dopamine attaches to these receptors it causes a *reduction* in dopamine release.)

Any dose of amisulpride is going to cause more dopamine to be released from these cells by blocking these autoreceptors and "tricking" the cell into releasing more dopamine. However, as the dose of amisulpride gets higher, it begins to bind to both the autoreceptors *and* postsynaptic receptors. Thus, more dopamine is still getting released, but amisulpride is also binding to those postsynaptic receptors and blocking dopamine transmission, so the released dopamine cannot really do much since it can't knock the amisulpride off the postsynaptic receptors. Thus the overall effect here would be a *decrease* in dopamine transmission, even though more is still being released. Generally, this is going to lead to sedation/cognitive and sexual side effects and the positives will be that it will help with schizophrenia and reduce anxiety. These effects are what led antipsychotics to first be labeled as "major tranquilizers", while benzodiazepines were later deemed "minor tranquilizers."

The reason for the efficacy of low-dose amisulpride in dysthymia is that the amisulpride binds to mostly just the autoreceptors and leaves the postsynaptic receptors alone, allowing the increased dopamine that has been released to naturally bind to the postsynaptic receptors and having the overall result of an increase in both dopamine release and transmission. I suppose the key in getting this medication to work for dysthymia is finding the "window" that has this overall effect, thus I believe the dosage should start out really low and be moved up slowly until an effective dose is reached. However, dose should *never* exceed 200mg/d for the treatment of dysthymia.

I'm sure this was way more information than you wanted to know. ;-)

My intent in posting this was just to clear up any confusion regarding the drug's action because when I look on this board most people seem to be perplexed by it; now hopefully they can just be redirected to this post.. Unfortunetly, many pdocs (esp. in the USA) have never even heard of this medication and can provide little help so I realize this board is the only resource for many patients.

scott


Share
Tweet  

Thread

 

Post a new follow-up

Your message only Include above post


Notify the administrators

They will then review this post with the posting guidelines in mind.

To contact them about something other than this post, please use this form instead.

 

Start a new thread

 
Google
dr-bob.org www
Search options and examples
[amazon] for
in

This thread | Show all | Post follow-up | Start new thread | FAQ
Psycho-Babble Medication | Framed

poster:scott-d-o thread:297519
URL: http://www.dr-bob.org/babble/20040109/msgs/300303.html