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HT5 Receptor types respond to dmt differently !

Migrated topic.

El Ka Bong

Rising Star
OG Pioneer
Look what I found - that makes me reconsider that idea that we all have a different trip on dmt every time, based on the time of day, and therefore how many serotonin receptors you have up and running - There are 5 or more types of 5HT / serotonin receptors, that can all vary in amounts in your body ...

And another article -

It quotes Strassmann's work apparently - so maybe it's old news,

"It is reported that the 5-HT1A and 5-HT2A receptors produce opposing cellular
responses and are often expressed on thesame cell [51]. In a subsequent study, Strassman
[24] used pindolol, a 5-HT1A antagonist, in combination with a sub-hallucinogenic dose of DMT (0.1mg/kg IV) and found a two- to three-fold enhancement of DMT’s effects (according to theHRS). Thus, it appears that the 5-HT1A is suppressingDMTs hallucinogenic activity."

...this means that another tryptamine extracted with dmt could act as a 5HT1A-blocker, enhancing the effects of dmt on 5HT2A's, and not acting as a MAOI at all.

... I do really believe it's all about our receptors that are present, as they are the 'levers' and 'locks' while dmt is just the "key" ... We are all born with a unique, genetically determined 'mix' of 5HT receptor types, that varies all the time, based on many things.

For eg - what if you have less 5HT1A's around in the night time - how would your trip go..?! Do we have more 5HTA1's made in teh morning than 5HT2-types?
It'd be interesting to do a case study of this, having someone launch at prescribed times of day, everyday for a certain length of time, all the while keeping detailed trip reports (as much so as possible anyway). A review of these reports would thus allow us to identify patterns in the trips and possibly correlate to levels of the 5HTAs. Although this would be rather longitudinal and entirely ungeneralizable, it would still provide interesting insights :D
Yes! Sorry to bump an old thread, but this thread has great potential.

How does the up-regualtion or down-regulation of 5-ht receptors affect a psychedelic experience, or even everyday life? Doctors and patients are constantly playing with the density and effectiveness of serotonin receptors. Does a brain with an above average density or number of serotonin receptors make you a more "psychedelic person" or a person capable of a different experience compared to others?

I'm been thinking about this when considering using chantix to "down-regulate" my nicotine receptors. Do daily users of ssri's notice a down regulation? Is this simply a tolerance build-up?

Is there a doctor in the house?:lol:
Ayahuasca definitely modifies the serotonin systems in the brain, and frequent work with the medicine over an extended period of time has increased my sensitivity to all kinds of compounds drastically.

I have read that Ayahuasca actually increases the number of serotonin receptors measured on platelets in the blood stream of long term users. I would be willing to bet that this phenomenon occurs within brain and other nervous system tissues as well.
DMT binds to a LOT of receptors in standard doses. (Scientific note here: We currently know of 13 different serotonin receptors.)

Here are some binding affinities given in npKi form. Fellow neuropsychology lovers, you have my sympathy for being interested in this article: Psychedelics and the Human Receptorome.

Ki is a standard way of measuring binding affinity. pKi is a logarithmic measure of that. It's like in chemistry where you can measure H+ ion concentration, and then the -log of H+ concentration is called pH. npKi is the normalized form of pKi: the receptor which is bound to most strongly is set at 4.00, and a Ki value greater than 10,000 is assigned an npKi of zero. This, an npKi of 3.00 means that DMT binds to this receptor 1/10th as strongly as it would at 4.00, but it's 10 times stronger than for npKi of 2.00. Most effects will thus come from values above ~2, which are the only ones I'll give.

I tried to format this so it looks pretty, but the forum won't keep all my spaces.

IMPORTANT NOTE: The study does not specify where DMT is agonistic, antagonistic, or inversely agonistic! That means we don't know whether DMT is turning the volume up or down at these sites, so to speak, unless I've found some other source that specified the nature of its activity.

5HT-7: 4.00 (antagonist)
5HT-1d: 3.97 (maybe agonist)
5HT-2b: 3.91 (agonist)
Alpha-2b adrenergic: 3.53 (probably agonistic at most of the adrenoceptors)
Alpha-2c adrenergic: 3.53
Dopamine-1: 3.51 (almost certainly agonist)
5HT-2c: 3.42 (almost certainly agonist)
5HT-1e: 3.28
5HT-6: 3.25
5HT-5a: 3.16
Imidazoline-1: 3.13
Alpha-1b adrenergic: 2.95
Alpha-2a adrenergic: 2.75
Alpha-1a adrenergic: 2.70
5HT 2a: 2.58 (agonist -- responsible for much of the psychedelic effects)
SERT: 2.37 (Serotonin transporter. Binds as a substrate, not an inhibitor like prozac.)
Sigma 1: 2.23 (Why do people say that it barely binds to this receptor at the concentration required to activate 5HT-2a?)

Higher doses of DMT will, of course, activate receptors lower on the list.

DMT also binds to other receptors which were not measured by this study.
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