Posted by KaraS on October 3, 2005, at 18:56:30
In reply to how to downregulate dopamine autoreceptors? ECT?, posted by iforgotmypassword on October 3, 2005, at 9:52:18
> sorry, i don't even know if i am using the word properly. :( i'm wondering what mechanisms cause dopamine autoreceptors to become less plentiful, and also what mechanisms cause post-synaptic dopamine receptors to become more plentiful.
This is exactly what I need to find out. A previous poster named King Vultan believed that if he flooded the relevant areas with dopamine, the autoreceptors would down regulate. He believed that Parnate did this for him. He felt kind of sick for a week at each 10 mg. level until his brain adjusted. The medication ended up working out well for him. His interpretation was that, among other things, it did down regulate his DA autoreceptors. He likened the experience to what happens when one takes an SSRI and it eventually forces down regulation in terms of SE. I don't know if he is right but I certainly hope so.
> i know ECT causes "downregulation"* of dopamine autoreceptors. is it the only means? and some antidepressants (desipramine and fluoxetine, and presumably other ADs like venlafaxine) cause increased "expression" of dopamine receptors. what does "expression" mean?
I'm not sure why you're including fluoxetine or venlafaxine here. Fluoxetine is mostly serotonergic. It has some NE increase but I would think that would be way overbalanced by the serotonergic effect. Same for venlafaxine. In addition venlafaxine has some small dopaminergic effect at high dosages but again, it's mostly serotonergic which is the enemy when trying to increase dopamine. I don't presume to understand all of this so maybe you are on to something that I don't comprehend here.
> *sorry if i am not using the word properly. is this the actual proper use?
>
> it seems like this would be one of the more important ways to keep the actual prefrontal and dopamine system healthy without causing tolerance would be to actually enhance the physical receptor balance rather than just increasing the flow of monoamines that may have nowhere to go when they reach certain nerve cells and areas of the brain (like the case possibly with MAOIs?). i'm just making this up, but i am very poorly coordinated physically (including with balance, and fine motor skills especially) it would seem the best way would be to adapt my brain to function better anatomically so extra dopamine (and/or NE, ACh) could actually be used properly. could certain ADs or even only ECT be the only methods that are capable of doing this?
Good question. Hopefully someone else can add some answers.
> i am extrapolating all of this so it may all be totally of the mark, but if anyone knows what im getting at, could you give me a good idea of how things work?
k
poster:KaraS
thread:562265
URL: http://www.dr-bob.org/babble/20051003/msgs/562439.html