WAY-100635

[anxietor]

WAY-100635, a drug that reverses fluoxetine-induced sexual dysfunction in rats, has been available for purchase for 3 months or so. Here's the purchase link: http://tht.co/product/way100635/ found in a reddit thread regarding PSSD.
"Acute administration of the 5-HT(1A) antagonist WAY-101405 resulted in a complete reversal of chronic fluoxetine-induced deficits on non-contact penile erections at doses that did not significantly alter baselines. Chronic co-administration of the 5-HT(1A) antagonists WAY-100635 or WAY-101405 with fluoxetine prevented fluoxetine-induced deficits in non-contact penile erections in sexually experienced male rats."
http://www.ncbi.nlm.nih.gov/pubmed/19435548

Has anyone tried it yet? I know it's very expensive.

[scot]

Cannabidiol
http://temple.pure.elsevier.com/en/publ ... c7f59ca88e).html

[anxietor]

Not sure about cannabidiol. I agree that taking WAY-100635 may have risks we don't know about.

Some people say that 5ht1a agonists are the answer rather than antagonists. I'm not sure if a consensus has been reached regarding that. I'm too paranoid to start experimenting.

I should mention that I have no idea whether tht.co is legit or not.

[scot]

I have found a lot of natural agonists but not antagonists.

[anxietor]

I don't know of any studies on the matter. I've just heard anecdotes. There doesn't seem to be any one treatment that works for everyone. Maybe some people would react better or worse to agonists/antagonists based on their unique brain chemistry?

[scot]

http://www.maps.org/news-letters/v21n1/v21n1-21to22.pdf

[Ghost]

The Jury is still out on which would work better. I've seen evidence for both. IDEALLY, we'd have an agonist that acted only in the Raphe Nuclei (RN), where all of out autoreceptors (and no post-synaptic heteroreceptors) are located. The RN innervates the rest of the brain (mostly the frontal cortex and hippocampus). That being said, I've found increased evidence that there are many receptors other than the 5ht1a that are downregulated with SSRIs. It's really a big fucking mess. The more you learn, the more confusing it all seems.

[scot]

Serotonin agoninsts.

Vitamins
http://forums.narcolepsynetwork.org/ind ... e/?p=27544

[r4ndom]

If someone can tell me what the dosing would be for a human and how to calculate this and the proper way to administrate it, I will order it and try it, I am going to do everything to eradicate this, the solution is out there.

[iggy131313]

As far as I can see it depends if you want a treatment or a cure....an agonist at the 5ht1a receptor is a treatment, but long term could lead to more downregulation and therefore a worsening of the situation

An antagonist should make you feel worse but with a long term aim of actually reversing the alterations and curing the situation so once the antagonist is withdrawal and upregulation has happened the brain is back to something close to pre ssri levels

We see it with the guy who took zinc,made him feel worse, it's a 5ht1a antagonist somatodentrically, made him more blunted, but whine he stopped he had a period of time where his symptoms stopped......zinc is a weak antagonist but it obviously did enough to cause a small amount of upregulation, which was sadly transient .....it could take years for the upreg to happen, if you look at tardive dyskinesia and antipsychotics, with a weaker blocker on dopamine receptors the chance of developing td is less and takes a few years....we are talking about the same thing, causing upreg using an antagonist....however a strong drug like haloperidol causes td almost instantly in many cases because of the power of it's antagonism at dopamine receptors,,,,,a powerful enough antagonist at somatodentritic 5ht1a receptors and one that was highly specific to that would reverse the downregulation.

From 4 years of constant study on the brain and it's receptors this is pretty logical.

Another example is a guy who has the same kind of damage as me, which I believe to be a severe chronic upregulation of 5ht2a receptors, he found that taking high levels of zinc and magnesium combined would reduce his suffering....this could have been due to the glutamate blocking abilities of both these combined, or perhaps other mechanisms, but if we speculate that it was the glutamate blocking......this worked for him for 2 years, if he missed a dose the akathisia would return....after 2 years the akathisia began to return anyway, at severe levels, he stopped the zinc/mag and it got even worse.....he tried to take the zinc/mag and this time the symptoms were made worse by it.....why?? It's pretty simple and we see it again with tardive dyskinesia....

After 2 years of constant use glutamate receptors compensated for the blockade of receptors by upregulating, it took 2 years for this upregulation to become once again enough to cause the akathisia to return (he would also have had other severely upreg receptors such as 5ht2a) stopping the antagonist allowed the blocked receptors to regain function making the situation even worse.......now he tries to apply the same blockers to those receptors and here is where we see the similarity to tardive dyskinesia treatment....when someone with tardive dyskinesia is given a dopamine antagonist to try and block the receptors and aliviate the over sensitivity to dopamine, it makes the matter worse, as the receptors are already so upregulated over the dopamine threshold that any further upreg makes the td worse....and dopamine antagonists cause further upreg.....that is what happened with my friend and his glutamate blockers, now when he took them, he experienced even more upregulation which heightened his symptoms.

It seems that receptors respond only to transmitter input, that and perhaps co regulation with other receptor. Types, they seems totally unaware that their number is too high...like a computer, they respond to instruction, but the instruction has to be correct....

For example, if my theory is correct on my own issue and I have a severe upregulation of 5ht2a...causing the severe akathisia and other symptoms, we know that 5ht2a increases glutamate and acts as a brake on dopamine release.....anything that causes dopamine release helps me, increase sing dopamine levels does nothing, as 5ht2a are brakes on the release.....only activities etc that cause the release but not the increase help me......now I have had severe dopamine inhibition for 4 years....after 2 years of this I develop tardive dyskinesia, showing the brain is trying to compensate for the dopamine inhibition by upregulating dopamine receptors, not by down regulating the 5ht2a....

The way I see all this is that we are playing a game of chess here with the brain being the grand master....every step we take, we have to anticipate the response that the brain will make...moves by us...counter moves by the brain.

And THAT is exactly why I feel for pssd and anhedonia, it's all about working counter intuitively to force the brain to make the correct adaptations. Upregulating somatodentritic 5ht1a receptors and therefore restoring dopamine release in the pre frontal cortex