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i didn't know trazodone was an SSRI at all » psychobot5000

Posted by iforgotmypassword on December 24, 2008, at 4:33:31

In reply to Re: Agomelatin: could 5HT(2c) action be bad for sl » Marty, posted by psychobot5000 on December 23, 2008, at 12:23:31

and i was hoping that the nefazodone SRI effect was weak enough that i wouldn't have to worry about it.

(sorry i just realized my whole post from here on in was my babbling about me and my nefazodone rx i hope to fill in the states, but want to post it to see if anyone finds it relevant and has a response.)

i have suspicions my problems are of the hyperserotonergic-hypodopaminergic domino effect type, and exacerbated by previous SSRI use. i am worried about increasing serotonin, i worry that i either have too much of it, or i am hypersensitve, or that i have receptor or transpoter genotypes i could benefit knowing more about, if it were possible.

i was under a faint impression that not only did 5-HT1a autoreceptor agonism decrease serotonin (an increase catecholamines), but that 5-HT2a antagonism did this as well (decrease serotonin, increase NE DA) and that 5-HT2c seemed to as well, but that it has complexities with regards to executive function (that it seemed to be the opposite of 5-HT2a in some ways).

i guess they may all be different in where their action is prominent. if i remember correctly (i may not), buspirone's anti-bruxism effect was due to its serotonin depleting and dopamine enhancing effect in the VTA. i *think* they tagged the mesocortical tract as being implicated in bruxism.

the final effect of nefazodone, and increase or decrease in serotonin, i am not sure of, and it bothers me. i know that the drug paradoxically increases REM by a small amount, whereas trazodone decreases REM, i think. i don't know the significance of this, if any, in determining what the broad chemical effect of nefazodone is.

both the hard to figure out SRI effect, and the 5-HT2c and mCPP issue bother me a lot. as does the 5HT-2b agonist property of mCPP, and how it's levels may depend on certain liver enzyme genotype(s) one has. (i think there was one or two enzymes that may be specifically relevant.)

the occupancy* of 5-HT2a by nefazodone is lower than i would have expected, making me wonder if it the recognition of nefazodone "having an effect" relied significantly on other properties of the drug, like its mCPP metabolite, or a possibility that it's SRI effect wasn't that weak at the dosage range that the drug ended up being rx'd at. but then again, i do not know what levels of antagonistic occupancy of 5-HT2a is associated with which types of responses.

i do not know anything about what type of occupancy profile trazodone has. it would be interesting to know how it compares, and which drug metabolizes into more mCPP at the dosage ranges that are used clinically.

* a single dose of 200mg nefazodone apparently creates ~39% occupancy of 5-HT2a receptors, and "less than 50% after 6 weeks of treatment with an average dose of approximately 450mg"


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URL: http://www.dr-bob.org/babble/20081223/msgs/870606.html