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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 9 of 9. This is the beginning of the thread.
Posted by blueberry on September 6, 2006, at 19:02:57
I wonder why dopamine agonists usually cause sedation. It seems like anything that is pro-dopamine would be stimulating. I wonder what mechanism is at play that causes dopamine agonists to be sedating. Maybe they slow down the release of actual dopamine? Dunno.
Posted by Phillipa on September 6, 2006, at 19:56:06
In reply to I wonder about dopamine agonists, posted by blueberry on September 6, 2006, at 19:02:57
Heah blueberry are you doing better. Been a while. Love Phillipa
Posted by jealibeanz on September 6, 2006, at 21:57:31
In reply to Re: I wonder about dopamine agonists » blueberry, posted by Phillipa on September 6, 2006, at 19:56:06
What are dopamine agonists?
Posted by Phillipa on September 6, 2006, at 22:09:38
In reply to Re: I wonder about dopamine agonists, posted by jealibeanz on September 6, 2006, at 21:57:31
Blueberry you're so smart I know you can explain it well. Love Phillipa
Posted by Tom Twilight on September 7, 2006, at 1:58:15
In reply to Re: I wonder about dopamine agonists, posted by Phillipa on September 6, 2006, at 22:09:38
Don't quite know why DA Agonists are such P*ss poor drugs, at least for most people.
There are of course exceptions!
If think its something to do with binding to dopamine auto receptors and so slowing dopamine release.
Eldopa can also be sedating to.Dopamine is really confusing!
Someone less tired and more knowlageble than me will explain it better!
Posted by Declan on September 7, 2006, at 3:36:57
In reply to Re: I wonder about dopamine agonists, posted by Tom Twilight on September 7, 2006, at 1:58:15
Is bromocriptine sedating? It wasn't for me, although there were side effects.
Cabergoline didn't do much(which was odd).
Deprenyl and Hydergine are both stimulating (and nice, for me).
Posted by linkadge on September 7, 2006, at 7:34:49
In reply to Re: I wonder about dopamine agonists, posted by Declan on September 7, 2006, at 3:36:57
When we consider 'stimulation' one must not attribute to dopamine what is really due to norepinephrine.
We don't really have any purely dopaminergic medications other than the dopamine agonists. Even when you take somthing like ritalin you are geting norepinephrine reuptake, and norepinephrine release. Tyrosine too, is the precursor to norepinephrine.
Norepinephrine is alerting while dopamine is more involved in motivation. A pure dopamine boost, may not affect energy as much as it increases interest. Increasing dopamine sometimes decreases locomotor activity. This is generally how ADHD medcations are thought to work.
Dopamine has both excitory and inhibitory actions. To confuse the matter, dopamine and norepinephrine are often released simultainiously.
Honestly, people become fixated on one particular neurotransmitter for no good reason. The number of people who come in here saying they have a dopamine problem is kindof silly. What is the basis for that, other than the idea that SSRI's don't work for them. Lack of SSRI efficacy is not really evidence of dopamine dysfunction. Some people who get a high from illegal drugs, conclude that they have a dopamine deficicancy. But that too is nonsensicle since everyone can get a high from illegal drugs, but not everbody has dopamine dysfuction. In essence, any drug that directly activates the pleasure centres of the brain, cannot really be used as a reliable indicator of biochemical workings.
Dopamine by itself is not the magic pleasure chemical. I've often thought that the combination of a dopamine agonist like mirapex, and a serotonin agonist like buspar, might be a good combination. People who take a dopamine agonist might simply be expecting the wrong thing. They may be expecting a buzz like what is provided by nicotine etc, but dopamine agonists do not directly activate reward circutry.
That being said, I knew a couple of people in school who did very well on dopamine agonists. They said it was not an energetic type of feeling at all, but that it increased interest. They basically said that they were able to sustain interest in things like reading or playing an instrument for a longer period of time.
Sorry for blithering
Linkadge
Posted by willyee on September 7, 2006, at 10:58:38
In reply to I wonder about dopamine agonists, posted by blueberry on September 6, 2006, at 19:02:57
> I wonder why dopamine agonists usually cause sedation. It seems like anything that is pro-dopamine would be stimulating. I wonder what mechanism is at play that causes dopamine agonists to be sedating. Maybe they slow down the release of actual dopamine? Dunno.
Yeah without being able to be technical,i have read over and over these two things,
--Dopamine can be both stimulative as well as inhibitory.
-- Gaba can be sedating,as well as stimulative.Too much gaba can greatly increase anxiety.
Makes finding help a lot easier eh,stinks.
Posted by yxibow on September 8, 2006, at 2:02:36
In reply to Re: I wonder about dopamine agonists, posted by willyee on September 7, 2006, at 10:58:38
> > I wonder why dopamine agonists usually cause sedation. It seems like anything that is pro-dopamine would be stimulating. I wonder what mechanism is at play that causes dopamine agonists to be sedating. Maybe they slow down the release of actual dopamine? Dunno.
>
> Yeah without being able to be technical,i have read over and over these two things,
>
> --Dopamine can be both stimulative as well as inhibitory.
>
> -- Gaba can be sedating,as well as stimulative.Too much gaba can greatly increase anxiety.
>
> Makes finding help a lot easier eh,stinks.
The manipulation of GABA can be anxiolytic, sedating -- but can also in too much amounts cause seizures rather than protect against them, which was and is the one of the many uses of benzodiazepines, and the more refined AED drugs that followed them.
Dopamine agonists such as carbidopa-levidopa (Sinemet/CR), primary treatment agents in Parkinson's, can even in an effective dosage range, produce psychosis. This is not surprising given the dopamine model of psychosis in schizophreniform disorders. Often patients have to take an amount of Seroquel (the agent with the least effect at D2 and pseudoparkinsonism outside of clozaril which may also be necessary as it has an even lower potential of D2 activity but requires expensive blood monitoring for low white blood cell count [2% mandatory discontinuation typical] and unpleasant side effects.)
This is the end of the thread.
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