Posted by SLS on September 15, 2012, at 19:34:45
In reply to Re: Pristiq dosages of 200 - 400 mg/day. » SLS, posted by phidippus on September 15, 2012, at 15:57:04
> One thing you can do is look into the neurotransmitters and the effects they have.
>
> "And what's the deal with clomipramine? Why is this SNRI considered more effective than any other, especially for treating melancholic depression? Calcium channel inhibition? Sodium channel inhibition? Sigma receptor stimulation? 5-HT2a receptor blockade? Muscarinic receptor blockade? NMDA receptor modulation? Opioid kappa and delta receptor stimulation? Glutamate receptor blockade?"
>
> say, for instance, sodium channel inhibition is shown to have negligible effects on mood. Sigma receptor stimulation results in inhibition of ion voltage gated channels-how this effects mood is unknown. NMDA receptor modulation may or may not affect mood, etc.
>
> Of course, all of these chracteristics could add up.
>
> The only thing we can't account for is the individual's reaction to any single medication
>
> In my case, Viibryd proved too be a more powerful anti-obsessional than Clomipramine was. What? Why?
>
> All I know is if a medication has 5ht1a partial agonism, I respond strongly.
>
> Eric
Tricyclics are also antiglutamatergic:"Although tricyclic antidepressants have been in existence since the 1940s when they were discovered upon screening iminodibenzyl derivatives for other potential therapeutic uses, their mechanism of action has remained unclear [A. Goodman Gilman, T.W. Rall, A.S. Nies, P. Taylor, Goodman and Gilman's The Pharmacological Basis of Therapeutics, eighth ed., Pergamon Press, New York, 1990]. In addition to their ability to hinder the reuptake of biogenic amines, there is mounting evidence that the tricyclic antidepressants inhibit glutamate transmission. Here, intrinsic tryptophan fluorescence spectroscopy is used to document the binding of desipramine, a member of the tricyclic antidepressant family, to a well-defined extracellular glutamate binding domain (S1S2) of the GluR2 subunit of the amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor. The binding is distinct from those of other known effectors of the receptor, including the endogenous sulfated neurosteroids pregnenolone sulfate and 3alpha-hydroxy-5beta-pregnan-20-one sulfate, and is consistent with a conformational change upon binding that is allosterically transmitted to the channel region of the receptor."
"Linking tricyclic antidepressants to ionotropic glutamate receptors" - Stoll, Gentile 2005
- Scott
Some see things as they are and ask why.
I dream of things that never were and ask why not.- George Bernard Shaw
poster:SLS
thread:1024121
URL: http://www.dr-bob.org/babble/20120912/msgs/1025745.html