Posted by fachad on February 20, 2003, at 0:42:09
In reply to maois and tca 's in relation to norepinephrine » fachad, posted by LAURA777 on February 19, 2003, at 16:24:34
Laura,
>all these drugs are norepinephrine enhancers ?? are they ??
That's a trick question. They both enhance and diminish NE functioning. It goes something like this:
TCAs (especially desipramine and nortriptyline) are powerful SNRIs. So an immediate effect of taking them is that there is more NE in the synapse. In that sense they enhance or increase NE.
However, with repeated administration (about 2 weeks, if I remember correctly), the nervous system adjusts itself to this by "down-regulating" the NE receptors. The NE receptors become less sensitive and there become fewer of them. So in that sense, TCAs diminish NE functioning.
That is a very simple example of a phenomenon that gets very complicated. Sometimes there are three or four known "downstream" effects of a drug.
This downstream phenomena makes it very difficult to say, "this problem is due to a (lack, excess, whatever) of (NE, DA, 5HT, GABA, whatever) and can be 'fixed' by taking this medication which (enhances, blocks) that particular neurochemical.”
Any drug you take has immediate effects, and downstream effects, and chronic effects. Also, sometimes a drug has one effect and its active metabolite has different or even opposite effects.
I believe that our way of thinking about psychiatric drugs has been influenced by the conventional medical model of bacterial infections and antibiotics. You just culture to find the specific offending pathogen, and then treat with agent that is known to be effective for that particular bacteria.
That works great for killing bugs, but is not an adequate model for altering and shaping the biologically based subjective experiences of human beings.
Here's a few more thoughts along those lines
http://www.dr-bob.org/babble/20020408/msgs/103154.html
> See my depression is different in that i do not suffer from insomnia or hypersomnia
Lucky you! Those are very hard to treat, especially if you have both.
>but my sympathetic is still in overdrive ..
I still think a beta blocker may be something to think about.
I also saw a reference tonight to using clonadine (an alpha adrenergic agent) in treatment of opiate addiction, somehow it lessened the suffering of those in withdrawal, and there was a known neurochemical pathway for this, something about DA and NE output in certain brain regions, but I can't find it now...
It may be worthwhile for you to look into alpha adrenergic agents used in treating opiate addiction, because opiate addiction and withdrawal may be a useful theoretical model for understanding your opiate relieved anhedonia.
poster:fachad
thread:138954
URL: http://www.dr-bob.org/babble/20030219/msgs/202061.html