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The Power Of Nature
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Discussion Starter · #1 ·
Tuning the serotonin systeem would be the perfect way to find a cure for social anxiety.
Some receptors cause good effects others cause bad effects, luckily there are several meds availible that work on those receptors, here's a list of available agonists and antagonists.

I will try a coktail soon, just gotta figure it all out a bit better.

5HT1A
Buspar
Tandospirone
Urapidil

5HT1x Agonism
Eletriptan (and all the other triptans, but eletriptan works on all serotonin 5HT1B-D receptors!!!)

5HT1D Antagonism
Ziprasidone
Ketanserin

5HT2C Antagonism (very important!!!!!!!!)
Agomelatonine
Remeron
Dotarizine
Ritanserin
Nefazodone
Trazodone
Dimebolin
Ketanserin
Pizotifen

5HT2A Antagonism
Nefazodone
Trazodone
Cyproheptadine
Pizotifen
Dotarizine
Ketanserin

5HT2A Agonism
Psychedilics which can be used as antidepressants in low doses, paradoxally so i'm not sure wheter 5HT2A antagonism is a must.

5HT2B Antagonism
Agomelatonine
Arsenapine
Lisuride
Ketanserin
Tegaserod

5HT3 Antagonism
Ondansetron
Memantine

5HT4 Antagonism
Piboserod
Lysine
Agonism
Metoclopramide

5HT6 Antagonism
Dimebolin
Ketanserin
Ritanserin

Agonism
Lisuride

5HT7 Antagonism
Pimozide
Ritanserin

There still are a few antipsychotics whith action at serotonin receptors, i'l add them in soon!!!
 

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Tandospirone
Urapidil

Good luck with finding them. I don't know about those other meds. You idea is good but getting them is another story ;) I hope you have a nice doctor.
Urapidil is cheap and available online (I won't post where of course because of board rules). It's the first time I have heard of that drug and I have no idea if it can be useful in the treatment of anxiety or depression.
 

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The Power Of Nature
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Discussion Starter · #3 ·
Tandospirone
Urapidil

Good luck with finding them. I don't know about those other meds. You idea is good but getting them is another story ;) I hope you have a nice doctor.
Yes i know those are rare but i added in everything thats availible, the rest should be easier to get tough.
Building a stack of those should cause major results!!

I was thinking of a
Buspar
Agomelatonine
Cyproheptadine
Memantine
Dimebolin
Low dose geodon (so it doesnt cause bad anti dopamine effects but only good serotonin effects!!)

Stack, It should work wonders!!!
 

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The Power Of Nature
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Discussion Starter · #4 ·
Urapidil is cheap and available online (I won't post where of course because of board rules). It's the first time I have heard of that drug and I have no idea if it can be useful in the treatment of anxiety or depression.
It works by agonizing 5HT1A receptors, so it should cause good effects, maybe not alone but very powerfull in a stack!!
A tuned serotonin stack in combination with deprenyl or something for some extra dopamine!!

I also find that 12 hours after i've taken MDMA i'm free of anxiety, i'm pretty sure its some serotonin receptors that has been massivly downregulated, still trying to figure out wich one.
 

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It works by agonizing 5HT1A receptors, so it should cause good effects, maybe not alone but very powerfull in a stack!!
I know that in theory such a med could be useful for anxiety, but if you type the two words urapidil and anxiety in PubMed you just get 6 hits and the abstract titles don't sound very relevant.
 

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The Power Of Nature
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Discussion Starter · #6 ·
I know that in theory such a med could be useful for anxiety, but if you type the two words urapidil and anxiety in PubMed you just get 6 hits and the abstract titles don't sound very relevant.
I dont beleive it would work on its own tough, i'm pretty sure you need the work on the whole serotonin system to get a great effect... Buspar on its own doesnt work all too great either but i beleive it could work great in combination with other things.

Thats why i looked on the web to find out what receptors should be agonised and what shouldnt be, with this list i could bould up some stacks and start some experimenting.

Also my anxiety is completely gone 12 hours after using MDMA, while GHB doesnt work for me at all (i can be fully high but still experience the same level of anxiety) so i think its my serotonin system.
I beleive some bad receptor is massivly downregulated 12 hours after MDMA wich causes me to feel good.

Agonize the good receptors and antagonize the bad receptors is the clue IMO, thats why srri's and buspar have limited succes while the serotonin system does seem to be very powerfull!!
 

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The Power Of Nature
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Discussion Starter · #7 ·
D2-antagonism, together with 5HT2A-blockade, may actually lead to 5HT1A-activation which in turn leads to more cortical dopamine: http://pt.wkhealth.com/pt/re/jneu/a...N3yrL7xn69qQ2NsWv!940204909!181195628!8091!-1.

So i've ordered risperdal (see study above, i want to take it in low enough doses so it doenst make someone tired and 5HT2A antagonism)
Buspar, see above after 5HT2A and a small bit of dopamine are antagonized 5HT1A is actived so adding buspar on it will add on to those good changes!!
Agomelatine for 5HT2C antagonism, wich has major benefits!!!
Ondansetron for 5HT3 antagonism
Metoclopramide for 5HT4 agonism (5HT4 agonists could be fast acting antidepressants!!!)
Tianeptine
Ritalin for extra motivation and social reward.

This stack should work great!!
 

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I had my first LSD experience in a long time about a week ago, too small a dose to get any visuals or psychedelic thinking (ie getting stuck in loops of thought), and while I didn't feel high or any physical sensation from it at all (obviously), I just felt amazingly happy and optimistic.

I'd love to get to the bottom of just exactly how it can produce such an intense antidepressant effect at such small doses. It seems the obvious answer would be activation of 5-HT1A but looking at which drugs are agonists and antagonists of this receptor, it's making very little sense to me.
 

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I had my first LSD experience in a long time about a week ago, too small a dose to get any visuals or psychedelic thinking (ie getting stuck in loops of though.
What exactly is this term "stuck in the loop" that people talk about with psychedelic drugs? I've heard people talking about it before, but never quite figured it out.
 

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Equilibrian Epicurius
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D2-antagonism, together with 5HT2A-blockade, may actually lead to 5HT1A-activation which in turn leads to more cortical dopamine: http://pt.wkhealth.com/pt/re/jneu/abstract.00005064-200103050-00026.htm;jsessionid=KgRH6hCcp77J3YkgG1RnYYbknnmXq0mHlRRN3yrL7xn69qQ2NsWv!940204909!181195628!8091!-1.
That doesn't seem quite right. 5-HT2A and D2 blockade work together to reduce dopaminergic neurotransmission, hence the efficacy of antipsychotics at treating schizophrenia and psychosis. However, at low doses, many antipsychotics actually increase dopamine by preferentially binding to dopaminergic presynaptic autoreceptors, thereby disinhibiting exocytosis of these neurons. Maybe they used low doses in that study.

Interestingly, 5-HT(2A) receptors were expressed on dopamine neurons in several A10 subnuclei that project to mesolimbic forebrain regions implicated in drug addiction, and recent evidence indicates that ventral tegmental area 5-HT(2A) receptor activation may modulate reward-related behavior in rodents.
*http://www.biopsychiatry.com/5ht2a-dopamine.htm

The increase in DA release induced by amphetamine (2 mg/kg i.p.) in the nucleus accumbens and striatum was significantly reduced by the selective 5-HT2A antagonist SR 46349B (0.5 mg/kg s.c.), but not affected by the 5-HT2C/2B antagonist SB 206553 (5 mg/kg i.p.).
*http://www.nature.com/npp/journal/v26/n3/abs/1395776a.html
 

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Yes
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It's really hard to explain. Psychedelics seem to have a very "cyclical" quality to them. Everything becomes apparent as a cycle, and when I talk about thought loops... it's difficult to explain. An example might be sort of like you start with an idea, reach it's conclusion, and then you start to realize the implications of that conclusion, which leads you back to that original idea... and you can spend a long time doing this and not realizing it lol

Not a particularly desirable thing, but usually only seen with stronger doses. I think it largely has to do with the fact that your working memory is pretty much non-existant. Kind of how they say a goldfish only has a memory of six seconds so by the time it swims around to the same part of the bowl again, it thinks it's new (although I know it isn't true, seems like an apt example.)
 

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Oh ok, I remember a weird phenomenon back in the day when I smoked weed, where people could talk to me and then about 3 seconds later their voice would sort of vanish and i'd question whether they actually said something to me or if i'd just imagined it, I assumed that maybe that was the loop. Did you ever experience that? I still to this day don't know what was going on with that.
 

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Yeah psychedelics do stuff like that a lot.

I was paid to play a computer game 4+ years ago as a "professional gamer," played once on LSD, and my team wasn't too happy with that because I wasn't sure if I was actually hearing sounds like footsteps or not. :lol
 

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The Power Of Nature
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Discussion Starter · #14 ·
It is interesting that some ppl use low doses of 5HT2A agonists as antidepressants, while in theorie those receptors should have a opposite effect. AMT and EAT where used/developped as antidepressants.
 

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The Power Of Nature
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Discussion Starter · #15 ·
That doesn't seem quite right. 5-HT2A and D2 blockade work together to reduce dopaminergic neurotransmission, hence the efficacy of antipsychotics at treating schizophrenia and psychosis. However, at low doses, many antipsychotics actually increase dopamine by preferentially binding to dopaminergic presynaptic autoreceptors, thereby disinhibiting exocytosis of these neurons. Maybe they used low doses in that study.

*http://www.biopsychiatry.com/5ht2a-dopamine.htm

*http://www.nature.com/npp/journal/v26/n3/abs/1395776a.html
Very interesting thank you for that post!!

Do you have more information about the other receptors? 5HT2C agonism is allways bad thats for sure, but i'm still unsure about the 5HT1x (exept 5HT1A) and 5HT3-4-6-7. Should they be agonized or antagonized? I tought antagonizing them is better except 5HT4.
 

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Yes
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The increase in DA release induced by amphetamine (2 mg/kg i.p.) in the nucleus accumbens and striatum was significantly reduced by the selective 5-HT2A antagonist SR 46349B (0.5 mg/kg s.c.), but not affected by the 5-HT2C/2B antagonist SB 206553 (5 mg/kg i.p.).
So if I do eventually get started on Dexedrine, it'd be wise to stay away from 5-HT2A antagonists?
 

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Equilibrian Epicurius
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Very interesting thank you for that post!!

Do you have more information about the other receptors? 5HT2C agonism is allways bad thats for sure, but i'm still unsure about the 5HT1x (exept 5HT1A) and 5HT3-4-6-7. Should they be agonized or antagonized? I tought antagonizing them is better except 5HT4.
I think you're right about all those (from what I remember reading), and I'm almost positive 5-HT6 and 5-HT7 are both anxiogenic. This looks like a great article with information on every serotonin subtype receptor:
http://www.acnp.org/g4/GN401000039/Ch039.html

So if I do eventually get started on Dexedrine, it'd be wise to stay away from 5-HT2A antagonists?
As long as you started the Dexedrine first then I don't see why you should stay away from 5-HT2A antagonists for the sole reason that they may attenuate amphetamine-induced dopamine release. You can always go off the 2A antagonist if you notice a decrease in Dexedrine's efficacy.
 

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So if I do eventually get started on Dexedrine, it'd be wise to stay away from 5-HT2A antagonists?
I would just consider taking an 5-HT2A antagonist like cyproheptadine in case of serotonin syndrome. ;)
 
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