Shown: posts 1 to 4 of 4. This is the beginning of the thread.
Posted by dondon on October 3, 2004, at 10:52:14
WHenever I take 5-ht2 antagonists with my zoloft, I always feel depressed. When I discontinue the 5-ht2 antagonists( remeron, trazodone etc. ) the zoloft seems like it's working again. I believev ssri's work partially by stimulating the 5-ht2 receptor , in my case anyways. The sexual side effects come from stimulation of this receptor.
Posted by Sad Panda on October 3, 2004, at 11:17:41
In reply to 5-ht2 receptor antagonists, posted by dondon on October 3, 2004, at 10:52:14
> WHenever I take 5-ht2 antagonists with my zoloft, I always feel depressed. When I discontinue the 5-ht2 antagonists( remeron, trazodone etc. ) the zoloft seems like it's working again. I believev ssri's work partially by stimulating the 5-ht2 receptor , in my case anyways. The sexual side effects come from stimulation of this receptor.
>
>Hi dondon,
What have you tried besides these two? Trazodone has a metabolite called m-CPP which can cause problems & Remeron is an alpha-2 NE antagonist which can be irritating. I think Nortriptyline is the ideal thing to add to Zoloft or Amitriptyline if Nortriptyline doesn't give you good sleep.
Cheers,
Paul.
Posted by King Vultan on October 3, 2004, at 12:08:42
In reply to 5-ht2 receptor antagonists, posted by dondon on October 3, 2004, at 10:52:14
> WHenever I take 5-ht2 antagonists with my zoloft, I always feel depressed. When I discontinue the 5-ht2 antagonists( remeron, trazodone etc. ) the zoloft seems like it's working again. I believev ssri's work partially by stimulating the 5-ht2 receptor , in my case anyways. The sexual side effects come from stimulation of this receptor.
I had the same problem taking trazodone while on Nardil. In my case, I believe this may be due to the issue of hypersensitive dopamine autoreceptors. Blockading 5-HT2A receptors releases dopamine, which should be a good thing, but in my case, certain drugs that release dopamine can either sedate or depress me. The hypothesis would be that the overabundant dopamine autoreceptors, which are inhibitory, react to the extra dopamine and slow down the firing rate of the neuron, causing depression and/or sedating. Nortriptyline did kind of the same thing for me, but it was not as bad as trazodone, probably because nortriptyline's strong blockade of norepinephrine reuptake provided enough of an antidepressant effect to offset the dopamine being released by its own 5HT2-A blockade.
This is only a theory arrived at by taking into account my reactions to the 12 different drugs I've tried, and I am not saying I have 100% confidence in it. There are other aspects of this that should perhaps be examined, as both trazodone and nortriptyline also blockade 5-HT1 receptors, an activity I tend to look very much askance at. Blockading presynaptic 5-HT1A presynaptic autoreceptors might be a good thing, but I fail to see how it could be good to blockade the postsynaptic 5-HT1A receptor, as this is the ultimate target for drugs such as SSRIs that work on serotonin--the idea is to cause stimulation of this receptor.
Todd
Posted by linkadge on October 3, 2004, at 13:05:31
In reply to Re: 5-ht2 receptor antagonists, posted by King Vultan on October 3, 2004, at 12:08:42
Thats actually what I wondered. Trazodone and Seroquel have listed properties as 5-h1a blockade. Does this mean they block the autoreceptor (good), ie pindolol/lithium, or block the 1a post synaptic receptor (bad) no neurogenesis.
Linkadge
This is the end of the thread.
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