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?
poster:iforgotmypassword
thread:562265
URL: http://www.dr-bob.org/babble/20051003/msgs/562265.html