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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 6 of 6. This is the beginning of the thread.
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.
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?
*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?
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?
Posted by Phillipa on October 3, 2005, at 18:21:45
In reply to how to downregulate dopamine autoreceptors? ECT?, posted by iforgotmypassword on October 3, 2005, at 9:52:18
Don't have a clue but would like to learn. Fondly, Phillipa
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
Posted by med_empowered on October 3, 2005, at 19:53:07
In reply to Re: how to downregulate dopamine autoreceptors? ECT? » iforgotmypassword, posted by KaraS on October 3, 2005, at 18:56:30
up/down-regulation can basically be done by flooding or depriving the brain of a given neurotransmitter. Sooo...lots of dexedrine, after a while, both reduces dopamine firing and causes downregulation as an adjustment to the continued presence of elevated levels of the neurotransmitter in the brain. This is why stimulant withdrawal sucks so much; suddenly, the downregulated brain is deprived of dopamine, and depression sets in (which usually goes away). Contrast this with antipsychotics...there's a definite up-regulation of dopamine there, especially with the old ones, as they adjust to a hypo-dopaminergic environment. This may be one reason for tardive dyskinesia, and its probably the reason for "dopamine supersensitivity psychosis" (ex: a non-psychotic patient given neuroleptic drug X for, say, bipolar disorder, suddenly becomes floridly psychotic on withdrawal; the problem is that her D2 system is super-sensitive to dopamine, and the absence of the neuroleptic is flooding the brain with dopamine, resulting in something kind of like an amphetamine psychosis). I don't think an SSRI would be the way to go for downregulation; the potent impact on serotonin reduces dopamine activity, unless there's a stimulant added. Is downregulation really what you want?
Posted by 4wd on October 8, 2005, at 22:41:54
In reply to Re: how to downregulate dopamine autoreceptors? EC, posted by med_empowered on October 3, 2005, at 19:53:07
> up/down-regulation can basically be done by flooding or depriving the brain of a given neurotransmitter. Sooo...lots of dexedrine, after a while, both reduces dopamine firing and causes downregulation as an adjustment to the continued presence of elevated levels of the neurotransmitter in the brain. This is why stimulant withdrawal sucks so much; suddenly, the downregulated brain is deprived of dopamine, and depression sets in (which usually goes away). Contrast this with antipsychotics...there's a definite up-regulation of dopamine there, especially with the old ones, as they adjust to a hypo-dopaminergic environment. This may be one reason for tardive dyskinesia, and its probably the reason for "dopamine supersensitivity psychosis" (ex: a non-psychotic patient given neuroleptic drug X for, say, bipolar disorder, suddenly becomes floridly psychotic on withdrawal; the problem is that her D2 system is super-sensitive to dopamine, and the absence of the neuroleptic is flooding the brain with dopamine, resulting in something kind of like an amphetamine psychosis). I don't think an SSRI would be the way to go for downregulation; the potent impact on serotonin reduces dopamine activity, unless there's a stimulant added. Is downregulation really what you want?
Do opiates affect the release of dopamine and the function of dopamine receptors? Specifically hydrocodone.
If one abused hydrocodone periodically over a long period of time could dopamine receptor function be affected, causing depression/anxiety either/both while still using and for months after stopping?
I've wondered about this a long time and looked for answers but never found one.
Marsha
Posted by tidge on October 12, 2005, at 7:40:00
In reply to Re: how to downregulate dopamine autoreceptors? ECT? » iforgotmypassword, posted by KaraS on October 3, 2005, at 18:56:30
hi everyone!
do you think that mirapex would be a good option for us major depressives? From what i know it is dopamine...
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