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onedayillsailagain

5-HT2B receptors are required for MDMA-induced hyperlocomotion and 5-HT release in vivo and in vitro.

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Was looking in to Metadoxine (a 5-HT2B antagonist) and came across this:
 

 

Here we show that acute pharmacological inhibition or genetic ablation of the 5-HT(2B) receptor in mice completely abolishes MDMA-induced hyperlocomotion and 5-HT release in nucleus accumbens and ventral tegmental area. Furthermore, the 5-HT(2B) receptor dependence of MDMA-stimulated release of endogenous 5-HT from superfused midbrain synaptosomes suggests that 5-HT(2B) receptors act, unlike any other 5-HT receptor, presynaptically to affect MDMA-stimulated 5-HT release. Thus, our findings reveal a novel regulatory component in the actions of MDMA and represent the first demonstration that 5-HT(2B) receptors play an important role in the brain, i.e., modulation of 5-HT release. As such, 5-HT(2B) receptor antagonists may serve as promising therapeutic drugs for MDMA abuse.

http://www.ncbi.nlm.nih.gov/pubmed/18337424

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Visual had had success with cabergoline which is an agonist of this. I hope to try it soon as well as I respond well to dopaminergic agents.

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There isn't much available for antagonizing 5-HT2B receptors.  The stimulating (agonist) of this receptor can be a problem.  And most ergots do this.  "The 5-HT2B receptor stimulation can also lead to pathological proliferation of cardiac valves fibroblasts, which with chronic overstimulation of 5-HT2B can lead to a severe valvulopathy." -- https://en.wikipedia.org/wiki/5-HT2B_receptor

 

I take cabergeline to stimulate (agonize) D2 receptors.  Unfortunately it has the above problem when taken long-term at large dosing.  Lite dosing seems safe but defining 'lite' and 'safe' over the course of decades is problematic.  So while it can be useful to try the med to see if it will help, if it is substantially helpful, then one has to navigate the long term risk.

 

Both documenting symptoms that tend to be D2 related and genetic testing for D2 related genes (such as rs1800497) can be helpful whether such a risk is justifiable.

 

 

In the end, since it has been reported that the majority of people recover from HPPD, it is good to wait before messing with meds unless things like anxiety are out of control.

 

HPPD tends to run in a few categories:

 

1  Learned behavior (plasticity) - by taking recreational drugs, one teaches the brain to 'trip'.  You asked for it so the brain is giving it to you

 

2  Underlying instability/weakness - drugs, stress, or whatever was sufficient to degrade the balance of communication between neuronal systems such as visual processing

 

3  Actual brain injury - an assault actually has caused sufficient damage to neurons and/or cognitive processing symptoms to render them 'wacky'

 

Whatever the reason, time and healthy living are ones best friends.  Ideally meds should be like a cast or crutch for broken bones that are only needed for a while.

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