Posted by zeugma on March 7, 2004, at 20:54:45
In reply to Re: Question about noredenic receports (smart people) » linkadge, posted by King Vultan on March 7, 2004, at 18:04:26
So here's another question about noradrenergic receptors... a stidy I read recently about how imipramine corrects HPA axis dysregulation speculated that it did so by lowering levels of norepinephrine through agonism of the alpha-2 receptor which is inhibitory. But I have gotten a powerful boost in antidepressant effect by adding buspirone to a TCA and Strattera. One of buspirone's effects is alpha-2 antagonism, which would raise synaptic levels of NE (actually a metabolite does this); if this hypothesis about how TCA's correct HPA axis imbalances is on the right track (and assuming I have this imbalance, which is plausible enough) wouldn't adding buspirone or Remeron dysregulate things further?
This is the relevant passage from the article:
The mechanism by which imipramine decreases CRH secretion is uncertain. Imipramine blocks reuptake of norepinephrine into presynaptic neurons. In brainstem regions such as the locus coeruleus, which contain inhibitory -2 autoreceptors (27), accumulation of norepinephrine at the synapse would decrease the firing of noradrenergic neurons. Because norepinephrine is excitatory to CRH release (28), an imipramine-induced decrease in brainstem noradrenergic activation could contribute to the findings reported here. We cannot, however, rule out the possibility that the anticholinergic or antihistaminic effects of imipramine, or an indirect effect, could also account for these findings.
Here's a link to the whole article.
http://jcem.endojournals.org/cgi/content/full/82/8/2601
poster:zeugma
thread:321715
URL: http://www.dr-bob.org/babble/20040304/msgs/321809.html