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The Big & Dandy 2C-B Thread - Stage 1

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never had the chance to try 2cb. all ive done is 2ce and 2ci seems like noone will make it and the only ppl to get it from are rc vendors
 
ungelesene_bettlek said:
but MDMA releases serotonin, which agonises the 5HT2A receptor. both MDMA and 2C-B cause more action on the 5HT2A receptors, which could lead to downregulation and therefore cross-tolerance.
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I am defintely no chemist (as is probably becoming obvious) but why would serotonin agonise the receptor? Its (the 5ht molecule) 'designed' to fit in the synpase there; thus allowing neurotransmission.....Meh, I should shut up. I think the cross tolerance issue is not between 5ht and 2C-B but the weak action of MDMA at 5HT2a; but it is VERY weak....I think. :\8)%)8o:D
 
ungelesene_bettlek said:
because serotonin is made to agonise serotonin receptors?
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Well, serotonin isn't made to agonise receptors; its 'made' to enable transmission over certain synapses. If serotonin agonised 5HT receptors, why for are we not hallucinating right now?
 
swilow said:
Well, serotonin isn't made to agonise receptors; its 'made' to enable transmission over certain synapses.
Click to expand...
As I understand it, these two statements are essentially equivalent.

If serotonin agonised 5HT receptors, why for are we not hallucinating right now?
Click to expand...
Because serotonin fully agonises 5HT receptors in the 'expected' way, in the 'expected' amounts (i.e. what the 5HT receptors are evolved to deal with), whereas psychedelics produce partial agonism at 5HT receptors, perhaps in unexpected amounts or in unexpected areas of the brain, thus producing all sorts of weird subjective effects.

I may be wrong about the above; neurotransmitters aren't my area of expertise..., but the above is the impression I had.
 
^ Well said.

serotonin agonizes 5-HT receptors which is the same as enabling transmission over certain synapses. Psychedelics change the way the receptor is agonized. They agonize the receptor but in a modified way from serotonin which causes the funky effects. Because the psychedelic is similar to serotonin in structure it fits into the receptor but since it isn't exactly the same structure as serotonin it doesn't agonize the receptor in the same way.
 
swilow said:
Well, serotonin isn't made to agonise receptors; its 'made' to enable transmission over certain synapses.
Click to expand...
yes, and this transmission in serotonergic synapses is made by releasing serotonin from the presynaptic part, which goes over to the postsynaptic part and agonises the serotonin receptors there.

btw, if that hasn't become clear yet: 5HT stands for 5-hydroxy-tryptamine, which is serotonin.

swilow said:
If serotonin agonised 5HT receptors, why for are we not hallucinating right now?
Click to expand...
I'm not really certain about that myself, but it is probably due to the mechanisms invert has already speculated about: maybe it is because classical psychedelics are specific for the 2A subtype of serotonin receptors, and maybe they are much stronger agonists there than serotonin itself. I don't think that they agonise receptors in a different way than serotonin like uniter writes, but I'm not sure about that either; maybe someone with deeper understanding can enlighten us.
 
invert said:
As I understand it, these two statements are essentially equivalent.
Click to expand...

I meant to write "correct transmisson", but yeah- they are the same. :\ 8o:D


ungelesene_bettlek said:
I'm not really certain about that myself, but it is probably due to the mechanisms invert has already speculated about: maybe it is because classical psychedelics are specific for the 2A subtype of serotonin receptors, and maybe they are much stronger agonists there than serotonin itself. I don't think that they agonise receptors in a different way than serotonin like uniter writes, but I'm not sure about that either; maybe someone with deeper understanding can enlighten us.
Click to expand...

I think that psychedelics have a greater affinity for 5HT2a and other 5ht receptors then 5ht/serotonin itself, hence their ability to alter conciousness as perceived. So- my thinking is that if LSD binds better then serotonin, MDMA (a serotonin releaser) shouldn't exert tolerance over more traditonal psychedelics, because any 5HT in the 5HT2a synapse will be antangonised by LSD....?

Meh. :D
 
swilow said:
Well, serotonin isn't made to agonise receptors; its 'made' to enable transmission over certain synapses. If serotonin agonised 5HT receptors, why for are we not hallucinating right now?
Click to expand...

I expel this exact same cry of tragedy every single day!

But seriously though? I agree with previous sentiments that normal levels of serotonin and other neurotransmitters produce sober or normal consciousness even though there is nothing truly normal ... by agonizing 5-HT receptors. The term 5-HT receptor means that serotonin is supposed to bind there and agonism means induction of an effect by binding to it.
Psychedelics and many other drugs work by mimicking neurotransmitters and agonizing 5-HT receptors in a stronger fashion but in selective patterns (not treating all 5-HT receptors equally) thereby inducing stronger signals than normally. Antagonist bind to the corresponding receptors as well! But they neglect producing the signal normally produced.
The reason serotonin doesn't produce hallucinations under normal circumstances is indeed that it functions as the norm / the transmitter that is supposed to bind to the 5-HT sites. But there are enough people who have psychological issues caused by chemical imbalances so you can expect them to have more activitity by more serotonin in some regions.

I think if you meditate and shut off input from your surroundings you change your 'gain', because activity is willingly decreased and balanced this way. But I think to compensate your brain increases serotonin levels so they return to average... which is why after much meditation you can see, hear and smell more and sharper (I've experienced this first-hand). That has to be an effect LSD and meditation therefore have in common and also why with meditation your brain handles this more naturally and steadily tuned.

I don't mean to sound like an expert and to clarify: I have a background in chemistry and not in medicine.
But what I personally think is that this is the simplified mechanism behind it.
 
^Best of posting in the regional forums, or looking about on pillreports :)
 
anamnesis, check the regional pill discussion thread in NSASDD. I didn't see your post, I just replied to it now.
 
well that thread sems to suggest the blue ones are 2c-b and the purple ones are something else.
i guess it depends which ones you have.
 
Ate them with my girl. I believe I was told the truth when it comes to what these tablets are.
 
another dosage question:

my friend and i both ate 20 mg of 2CB HBr salt i believe back in may
i had experimented with 2ce from 12-20 mg, acid and mushrooms a few times
and my friend had eaten mushrooms and L, but no other psychedelic.

we both found 20 mg to be underwhelming
i only have 60 mg left, so we are both gonna take 30 mg this saturday
i realize jumping the dose 10 mg might be a lot, but then again, 30 mg doesn't seem like too crazy high for this chem

what do you guys think?

also, i took 12 mg 2ce last saturday (one week apart exactly)
will i have any noticeable tolerance?
 
^ No tolerance issues, and you will probably be fine if you up the dosage to 30mg since 20mg was underwhelming for you. It makes sense since you only have 60mg left. This substance is generally quite forgiving.
 
Ya, if you're looking for a real trip take 30. 25mg for me was nice but didn't quite propel me to where I wanted to be, next time I do it I'm taking 30mg
 
sweetness, thanks for the quick answers

i'm also getting some ketamine for free maybe before the music fest this weekend. i've never tried K, so we'll probably do it by itself, but i wonder how K combines with 2cb or -e.

or how -e and -b combine

i never combine any psychedelics unless weed counts
 
bac kto the drawing board!

hello hello

monkey and i have been playing lots of learning games recently and i think we're getting to the stage of needing outside input. we've experimented with 2c-b in doses ranging from 5mg insufflated to 40mg orally, as well as combining with lsd mdma dmt and others, had previously left sourcing to monkey's uncle who now has no intention of continuing our arrangement. guess it's back to the theoretical drawing board for some chatterboxing. i'm new on the forum so bear with me if i break any rules - correction/advice welcome - pm me if you like....

so then - actual questions ;-)

how do i tell hbr from hcl?
what's the deal with redosing - theoretically does taking it today mean that monkey will not feel the effects of taking it tomorrow?
is it feasable to dissolve say 150mg in 100 drops of any liquid and dose orally @ 15mg per drop? i understand that the answer to this is dependent on which salt it is so answers in either case would be useful!

thanks!
love and light
 
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