Posted by linkadge on June 19, 2005, at 16:00:55
In reply to Re: Who knows the drug synergy mechanism? » SLS, posted by linkadge on June 19, 2005, at 15:16:57
Oops, I wrote that above post without even knowing you guys were already ahead on the buspar/pindolol combination.
The problem is that it is so weird the way these drugs affect people.The term "serenics" has been used to describe post synaptic 5-ht1a agonists, because they have anti-agressive actions. But as SLS mentioned, these agents can promote anxiety. But they also have antidepressant action.
It's really dumb, because one doctor says low serotonin causes anxiety, and another says high serotonin causes anxiety.
This is what I think. I think an initial serotogenic challence causes an initial anxiety, but then produces a subsequent change in an organisms coping stradegy. (The reason I say this is because post-synaptic 1a agonists cause an acute increase in hippocampal proliferation) This effect I think is what is responsable for the "anti-panic" effect of the drugs. So its almost like the drug induced anxiety reduces the impact of an environmental anxiety.
But then SSRI's may help anxiety independant of all of this serotonin nonesence as it has been found that all of them inhibit the enzyme that metabolizes allopregnalone, a potent gaba-ergic neurosteroid, enhancing its acton some 20 fold.
But then there are other findings that say that "too much" serotonin at other receptors can cause agressiveness. I read a few studys that suggested when SSRI's were combined with pindolol there was an agressive reaction.
I personally found that lithium (5-ht1 autoreceptor antagonist) and a SSRI made me feel very ANGRY where neither alone cause any of those feelings.
Personally, if you ask me, I think that I have supersensitive serotonin autoreceptors. Of course I have no way of knowing. Some pindolol might sort that out.
I have also thought that pindolol and lithium would be interesting. Lithium is a 5-ht1b autoreceptor antagonists. Both the 5-h1a/b autoreceptors serve to reduce overall serotogenic tone when activated.
Then again what would lithium and buspar do? Since lithium is not a 5-h1a autoreceptor antagonist, but a 5-ht1b autoreceptor antagonist.
How many people on lithium would do as well on a selective 5-ht1b autoreceptor antagonist, without all the extra inositol depleating effects of lithium. I think 5-ht1b autoreceptor antagonist have a strong, "I'm not going to set myself on fire, and jump infront of moving traffic" actionExercise and Shocktreatment and rTMS seem to reduce the sensitivity of the 5-ht1a/b autoreceptors.
Post-synaptic 5-ht1a agonism also reduces acetlycholine release, which may have functionality at the cholinergic/adrenergic axis.
But in some ways ginkgo worked well for me, which is why I'd like to try tianeptine. Ginkgo serves to accelerate 5-ht uptake and also as a fairly potent 5-ht1a post-synaptic agonist.Depressed people have elevated 5-ht2 receptors, but it is interesting to note that post-synaptic 1a agonism is sufficiant to down-regulate the 5-ht2 system. So might not really be direct 5-ht2 agonism that downregulates the 5-ht2 system, which is probably why TCA's downregulate the 5-ht2 system even though they're 5-ht2 antagonists.
But there is such a ballance between the serotogenic system and the dopaminergic system. SSRI's might just serve to even out the ying-yang a little.
But the dumbest thing that I recently read was this. They recently found some sort of depression gene. A short-short varient of the 5-ht transporter. Anyhow, this particular gene codes for a SLOWER serotonin reputake !!. So what good does it do by pumping these individuals full of drugs that serve to futher slow their already slow reputake system???
So I personally prefer the term "placebo's with a buzz"
Linkadge
poster:linkadge
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URL: http://www.dr-bob.org/babble/20050617/msgs/515573.html