Another attack like that will result in a lifetime ban. Last warningpterostilbene wrote: ↑Wed Jul 08, 2020 2:15 pmThis is no research, you russian mental case, this is a remark on your intellectual shortcoming and corruption. If you come with random bullshit propositions (truly absurd, weak ones besides), it is your obligation to make a case for them instead of waiting for others to disprove them. Basically you're acting like an insignificant troll ever, and your egocentric issues in your pathological behaviour are clear to see.
You seem to think there would be a primitive, clear-cut difference between good and bad in 5HT2A receptors. Which one can only think if one has read nothing at all about the topic (including what I posted in the beginning), and besides understands almost nothing at all about PSSd-related issues, and prefers to make things up oneself.
If 5-HT2A didn't ever feel good (by increasing dopamine in some areas, as one can read), I would never have focused on it as possibly being positive.
Currently don't have more time, but I'll get back to your bullshit.
5-HT2A Desensitization Reduces Glutamate Activity
Re: 5-HT2A Desensitization Reduces Glutamate Activity
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Re: 5-HT2A Desensitization Reduces Glutamate Activity
Hardly automatically an error, and Ketanserin is highly selective at low and normal doses for 5-HT2A and only selective for 5HT2C at high doses according to Wikipedia. And "brain region specificity" will also be limited if it's specific...sylv wrote: ↑Sun Jul 05, 2020 4:45 pmThe one which lacks the brain region specificity and used an outdated, not selective enough to discriminate between 5-ht2a/b/c subtypes, radioligand Ketanserin ? The most of the older research on 5-ht2 were wrong in their findings due to the same error.
https://pubmed.ncbi.nlm.nih.gov/9342771/
One of the only few studies of St. John's Wort on 5-HT2C, in comparison to a deluge of mentions of 5-HT2A, mentions its constituent Amentoflavone, which is has extremely low bioavailability and exists only in low doses in John's Wort.
https://link.springer.com/article/10.10 ... 002-1073-7
No idea what is supposed to justify your approving nodding about non-selective DOI over sneering about Ketanserin here, but whatever, it's after all only about your fun and personal standing, isn't it.Their results haven't been replicated but actually contradicted in the endocrine response to 5-ht2 agonist. ( DOI used here is a non-selective like ketanserin, but at least the endocrine response is a valid functional assay of 5-ht2a ). That's the second reason why this single study in the rodent is not enough
https://pubmed.ncbi.nlm.nih.gov/12905103/
Maybe. There are always lots of minute details to take into account, I didn't suggest a different approach (e.g. the last study I posted spoke of complex interactions with other receptors), but some doubts in one direction don't mean an absolute certainty of another kind. Yet the latter is your standard approach in anything.Above all, 5-HT2 GPCR's, especially 5-ht2a, differs significantly in the regulation of their expression between humans and the rodents. It's regulation differs even within the specific brain region and cell type of the same species. Find more at (but not in the abstract):
https://pubmed.ncbi.nlm.nih.gov/12650852/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110590/
Not inaccurate or "failing", as stated above. And in any case, it is not something I invented or one can casually dismiss, much less with a casual remark about antipsychotic binding (which bind to anything and aren't conceptually clear in all details, the same as other things). This doesn't create a simple picture.Mostly by the older research which were quite inaccurate for the reasons stated above, like failing to discriminate between 5-HT2a, 5-HT2c subtypes and by using psychedelics (5-ht2a / mGLUr2 dimer agonists ) to induce OCD in the animal models"well proven" about 5HT2A no less is its involvement in OCD
Incidentally, the last study I posted about Flibanserin gave a similar picture of an "oppressive" or antisocial feeling from overly strong 5-HT2A, as one might suppose in OCD.
Here is a study about genetic association:
"Association of serotonin receptor 2a haplotypes with obsessive–compulsive disorder and its treatment response in Iranian patients: a genetic and pharmacogenetic study"
https://www.dovepress.com/association-o ... rticle-NDT#
If 5HT2A receptors enhance acetylcholine, that might be associatd with OCD:
"Activation of 5-HT2 Receptors Enhances the Release of Acetylcholine in the Prefrontal Cortex and Hippocampus of the Rat"
https://pubmed.ncbi.nlm.nih.gov/15266551/
And I haven't only tried St. John's Wort for 5-HT2A, but Salix Alba, from the after-effect of which I can find it plausible to 5-HT2A upregulation might be partly associated with OCD-like behaviour.
But f 5-HT2A, I will turn my attention elsewhere, I don't care until I find new clues about it or if something else influences it.
I have never seen like that and can't explain its various effects.
lAMO +
"It competitively inhibits absorption of serotonin, noradrenaline, and dopamine; it also downregulates presynaptic membrane-adrenergic receptor density and reduces binding of neurotransmitters to presynaptic membrane-adrenergic receptors, thereby increasing their concentrations in the synaptic cleft, mimicking the effect of antidepressants"
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4946846/
Quite a lot for accurately discriminating the effects to one receptor subtype ( from 20+ others ) through introspection?
Almost all studies mention the MAO-aspect at most in a dismissive manner, or pointing out its small effect focusing mostly on other things instead. It had also been disproven or "not replicated": "In fact, the MAO inhibitory effects of hypericin could not be confirmed in subsequent studies."
You seem to have forgotten that there are some receptors, aside from 5-HT2A, which gain particular attention in studies of St. John's Wort, especially 5-HT1A. And you seem to have picked pretty much the only study that makes a big deal of this effect.
It is indeed quite absurd to put MAO above all other actions, and contradictory to use my remark about effects on other receptors to point out the difficulty of picking out the effect of MAOi on many receptors (also when when I don't care about MAOi at all).
Don't presume on everything I might have done or read to make statements about a particular action, especially that of 5-HT1A antagonism, which very consistently causes dead/numb dick (even with erection), but improved symptoms afterwards.
I have mentioned linear effects and non-linear changes (in one way or another) to contraindicate how MAOi might be associated at all with certain effects, which is pretty clear with something like antagonism with upregulation. This doesn't even require introspection, but just the ability to distinguish changes over a period of time. This is also required by common-sense if one wants to determine any effects at all... Otherwise, forget the forum.
I know some have a hard-on for any kind of MAOi action, however it seems a silly effect to me, hardly bound to cause any useful - rather than detrimental, but by the way then less easily reversible - changes.
Weasel, start out by engaging with a thread in a non-hostile, non-arrogant and rational manner. That aside, Inositol's effects also don't seem to be good acutely, but rather after its most acute and strongest action seems to have worn off (similar to actinf on 5-HT2A and then causing downregulation - but be that as it may).By the way, Inositol is of course implicated in the PSSD, but in my opinion, if am allowed to represent one without being attacked, the side effects are more due to desensitizing the PKC - PI3K signal transduction
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Re: 5-HT2A Desensitization Reduces Glutamate Activity
Jaxx wrote: ↑Wed Jul 08, 2020 4:41 pmAnother attack like that will result in a lifetime ban. Last warningpterostilbene wrote: ↑Wed Jul 08, 2020 2:15 pmThis is no research, you russian mental case, this is a remark on your intellectual shortcoming and corruption. If you come with random bullshit propositions (truly absurd, weak ones besides), it is your obligation to make a case for them instead of waiting for others to disprove them. Basically you're acting like an insignificant troll ever, and your egocentric issues in your pathological behaviour are clear to see.
You seem to think there would be a primitive, clear-cut difference between good and bad in 5HT2A receptors. Which one can only think if one has read nothing at all about the topic (including what I posted in the beginning), and besides understands almost nothing at all about PSSd-related issues, and prefers to make things up oneself.
If 5-HT2A didn't ever feel good (by increasing dopamine in some areas, as one can read), I would never have focused on it as possibly being positive.
Currently don't have more time, but I'll get back to your bullshit.
I mean this only in the most personal way:You've always been an asshole, "Jaxx".
Re: 5-HT2A Desensitization Reduces Glutamate Activity
Cant express how little this means to me. Hope you stay away from this place as you only add negativitypterostilbene wrote: ↑Wed Jul 08, 2020 6:03 pmJaxx wrote: ↑Wed Jul 08, 2020 4:41 pmAnother attack like that will result in a lifetime ban. Last warningpterostilbene wrote: ↑Wed Jul 08, 2020 2:15 pm
This is no research, you russian mental case, this is a remark on your intellectual shortcoming and corruption. If you come with random bullshit propositions (truly absurd, weak ones besides), it is your obligation to make a case for them instead of waiting for others to disprove them. Basically you're acting like an insignificant troll ever, and your egocentric issues in your pathological behaviour are clear to see.
You seem to think there would be a primitive, clear-cut difference between good and bad in 5HT2A receptors. Which one can only think if one has read nothing at all about the topic (including what I posted in the beginning), and besides understands almost nothing at all about PSSd-related issues, and prefers to make things up oneself.
If 5-HT2A didn't ever feel good (by increasing dopamine in some areas, as one can read), I would never have focused on it as possibly being positive.
Currently don't have more time, but I'll get back to your bullshit.
I mean this only in the most personal way:You've always been an asshole, "Jaxx".
Re: 5-HT2A Desensitization Reduces Glutamate Activity
I am someone who can get an amazing window of recovery with SJW. It takes about 24 hours to have this effect, where I get emotions flooding back and my peni* feels alive again.
The same goes for Cyproheptadine... But cyproheptadine only works 4 days after a single 1mg dosage. WHY?!
Now, what I need help with is developing THEORIES, as to WHY CYPRO WORKS.
But it doesn't work when we dose it acutely.
In fact, a single dose of cyproheptadine (<1mg), will cause the following effects:
-Horrible libido.
-Fatigue.
-Ravenous appetite.
-Incredible digestion.
-Numbing of all my emotions.
BUT...... It's the REBOUND of cypro.... That CURES us of PSSD.
DAY 4 and 5 AFTER using 1mg of cypro, there's this incredible SNAPBACK effect....
Orgasm returns, no more blunted libido, everything amazing.
But WHY....
What is happening 4 days after Cypro?
I need help understanding how to replicate these effects.
My current theories are as follows:
1. Cortisol rebound (So how to test?)
2. 5-HT1A receptor modulation (So how to test?)
3. Histamine rebound?
The same goes for Cyproheptadine... But cyproheptadine only works 4 days after a single 1mg dosage. WHY?!
Now, what I need help with is developing THEORIES, as to WHY CYPRO WORKS.
But it doesn't work when we dose it acutely.
In fact, a single dose of cyproheptadine (<1mg), will cause the following effects:
-Horrible libido.
-Fatigue.
-Ravenous appetite.
-Incredible digestion.
-Numbing of all my emotions.
BUT...... It's the REBOUND of cypro.... That CURES us of PSSD.
DAY 4 and 5 AFTER using 1mg of cypro, there's this incredible SNAPBACK effect....
Orgasm returns, no more blunted libido, everything amazing.
But WHY....
What is happening 4 days after Cypro?
I need help understanding how to replicate these effects.
My current theories are as follows:
1. Cortisol rebound (So how to test?)
2. 5-HT1A receptor modulation (So how to test?)
3. Histamine rebound?
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Re: 5-HT2A Desensitization Reduces Glutamate Activity
<my usernameLokzo55 wrote: ↑Mon Aug 24, 2020 4:36 pm I am someone who can get an amazing window of recovery with SJW. It takes about 24 hours to have this effect, where I get emotions flooding back and my peni* feels alive again.
The same goes for Cyproheptadine... But cyproheptadine only works 4 days after a single 1mg dosage. WHY?!
Now, what I need help with is developing THEORIES, as to WHY CYPRO WORKS.
But it doesn't work when we dose it acutely.
In fact, a single dose of cyproheptadine (<1mg), will cause the following effects:
-Horrible libido.
-Fatigue.
-Ravenous appetite.
-Incredible digestion.
-Numbing of all my emotions.
BUT...... It's the REBOUND of cypro.... That CURES us of PSSD.
DAY 4 and 5 AFTER using 1mg of cypro, there's this incredible SNAPBACK effect....
Orgasm returns, no more blunted libido, everything amazing.
But WHY....
What is happening 4 days after Cypro?
I need help understanding how to replicate these effects.
My current theories are as follows:
1. Cortisol rebound (So how to test?)
2. 5-HT1A receptor modulation (So how to test?)
3. Histamine rebound?
5ht2a is the receptor. We need to upregulate it, or increase binding at this receptor.
SJW increases binding or upregulates it by 50% after chronic (months) usage.
Another user posted success with THC and Panax Ginseng. THX and Panax Ginseng also upregulate 5ht2a.
Sleep deprivation increases binding at 5ht2a greatly. I have rapid reversal of my emotional blunting and low libido after sleep deprivation.
Too much 5ht2a = schizophrenia.
People complain about DP/DR with mushrooms, shrooms stimulate 5ht2a. Probably too much stimulation and it internalizes the receptors or something. DP/DR is really just emotional blunting, I believe they are the same thing and it is caused by the 5ht2a receptor being blocked or lowered in activity.
Anti psychotics and SSRI = down regulate 5ht2a.
No sources but if you Google search anything I have written here you will find it to be true. There are heaps of studies on the above.
Cypro is a 5ht2a antgaonist, so initially it does the opposite of what we want, perhaps after it's gone from the receptor something happens and you have increased binding at 5ht2a.
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Re: 5-HT2A Desensitization Reduces Glutamate Activity
don't cells take 3 days to recycle??
schizophrenia has less 5ht2 and more 5ht7
and it's not so simple as upregulating this or that
for example upregulation of 5ht2a on gaba interneurons could blunt dopamine release
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Re: 5-HT2A Desensitization Reduces Glutamate Activity
Why do all anti psychotics block 5ht2a?PsychoGenesis wrote: ↑Sat Oct 24, 2020 2:19 pmdon't cells take 3 days to recycle??
schizophrenia has less 5ht2 and more 5ht7
and it's not so simple as upregulating this or that
for example upregulation of 5ht2a on gaba interneurons could blunt dopamine release
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Re: 5-HT2A Desensitization Reduces Glutamate Activity
Has anyone found any ways to increase 5-HT2A receptor sensitivity? Any medications which work for this?
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