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IlostaMadge said:
I mean, I offered to post something on blacklight to prove what I said, and instead of giving me the benefit of the doubt, 11 people pmed Hammilton asking for him to never let me post, that's depraved, insecure and disgusting, and the above remark by Furious George is a perfect example of that self centered psychological mechanism in action.
Nope. That's just the wish to maintain a certain standard at Blacklight. Everything you wrote in this particular thread so far was nonsense. If anybody would have asked Bluelighters before if they like to read such bunk they probably would have refused as well.

Murphy
 
I don't post, and I am unsure whether to do so or not in light (oh the irony) of the responses here.
Egotistical masturbation = insecurities about your own prowess within the field that make you deny that anyone could have superior understanding without a shedload of qualifications and respect in the field.

So, you post that you were delusional from ketamine and whatnot, and then you retract it? Why? So lying isn't an issue?

No one is rejecting what you say because you lack credentials- because no one here knew that until you said so, although your confusion of simple concepts makes this obvious.

People sending me PMs is neither depraved (are you familiar with the meaning?) insecure or disgusting. It's because we try to keep a minimum level of discussion which you're not begining to approach.

If you want to discuss egos, why not look at your own? Everything you're writing is based upon the messiah complex you've developed. You've somehow arrived at the conclusion that your few months of study were enough for you to figure 'everything' out. You're mocking everyone who actually worked to learn what they know. Yet you managed to figure everything out without any effort on your part whatsoever.

That's an impressive display of ego.

For someone who claims to have everything regarding serotonergic psychedelics figured out, you know so very little.

Things you've said recently that are nonsense:

BK MBDB by itself is a pure stimulant with high adrenaline facility and dopamine effects.

D2 burn out is the primary factor in stimulant binge mediated anxiety is it not?

MDMA won't cause primary noradrenaline release as it won't bind to the beta carbon electropositive site on the NEVMAT or reuptake site on the NET, it would be as a secondary function of it'a ability to antagonise both of these sites causing decreased reuptake and increased vesicle release akin to DA NEVMAT antagonism inspiring this mechanism.

MDMA won't cause primary noradrenaline release as it won't bind to the beta carbon electropositive site on the NEVMAT or reuptake site on the NET, it would be as a secondary function of it'a ability to antagonise both of these sites causing decreased reuptake and increased vesicle release akin to DA NEVMAT antagonism inspiring this mechanism.

(see: Psychopharmacology (Berl). 2007 Jan;189(4):489-503. Epub 2005 Oct 12. Links
MDMA (Ecstasy) and human dopamine, norepinephrine, and serotonin transporters: implications for MDMA-induced neurotoxicity and treatment.Verrico CD, Miller GM, Madras BK.
Department of Psychiatry, Division of Neurochemistry, New England Primate Research Center, Harvard Medical School, 1 Pine Hill Drive, Southborough, MA 01772-9102, USA.)

The compound, being far far too big (and having a double bonded ketone) to fit through a DA transporter should be almost un-neurotoxic due to not actually releasing harmful breakdown products, the idiotic length of that side change must change DAT conformation over time slightly, as many reports have said that is lessens the ability to enjoy amphetamines and other cascaders

I realise that my posts in the last apologies thread just turned into an egomaniacal rant. I guess there is only so much spam this forum can take.

(oops, that actually makes sense for a change!)

And this doesn't even get into the garbage you spew in the lounge.
 
I am truely sorry you feel this way Hammilton, I hope we can be friends again one day.
 
Everytime someone writes some ridiculously crazy drugged out crap on bluelight, a machine elf is born.

But let's stop the flaming here, I don't want to have to delete posts.
 
Would it be possible for all this negativity to be deleted along with the posts of mine that caused it?
It really has no place here, and I will leave ADD alone in future.
 
Scared others will see, and that you will no longer be able to pose as "A neuropharmacologist" on other sites with the same username Madge? Delete the lot, save some face, keep promoting the unknown as safe. Harm reduction my anus.

Nuke, I'm very sorry if I'm too close to flaming. But I'm really opposed to what Madge is trying to do, which is spread his nonsence as gospel to those who don't know better, in a cynical attempt to prevent a dip in sales.
 
There's a lot of relevant pharmacy in this thread so I don't want to delete all of it, but try to keep the insults to a minimum and provide refs for your conjecture.
 
before everyone gets too carried away with whether something is a substrate for one monoamine transporter or another it is worth bearing in mind that amphetamine type stimulants can get into the neuron straight through the extracellular membrane by passive diffusion. mostly salt form outside the neuron, the small amount of freebase (from the equilibrium salt salt solution at physiological pH) dissolves in membrane and reforms salt on inside. methamphetamine can get through this way.
the jury is out on 4-methyl methcathinone safety. I would expect that the betahydroxy metabolite has 'interesting' adrenergic effects.
 
Now this thread turned strange, indeed. Cut the crap and get to the cheese. If someone claims stuff like what's been claimed in this thread, I'm interested to hear the reasoning behind the claims. So, Madge, please do post your ideas when you're ready, so that they may be discussed.
 
vecktor said:
before everyone gets too carried away with whether something is a substrate for one monoamine transporter or another it is worth bearing in mind that amphetamine type stimulants can get into the neuron straight through the extracellular membrane by passive diffusion. mostly salt form outside the neuron, the small amount of freebase (from the equilibrium salt salt solution at physiological pH) dissolves in membrane and reforms salt on inside. methamphetamine can get through this way.

As a side note that may have escaped some readers, this is a big reason why nitrogen is so abundant in compounds with pharmacological action.
 
vecktor said:
before everyone gets too carried away with whether something is a substrate for one monoamine transporter or another it is worth bearing in mind that amphetamine type stimulants can get into the neuron straight through the extracellular membrane by passive diffusion. mostly salt form outside the neuron, the small amount of freebase (from the equilibrium salt salt solution at physiological pH) dissolves in membrane and reforms salt on inside. methamphetamine can get through this way.
the jury is out on 4-methyl methcathinone safety. I would expect that the betahydroxy metabolite has 'interesting' adrenergic effects.

The mephedrone-euphoria wears of quite quickly, but the methylphenidate-like stimulation carries on for an hour or two (or a bit more if taking a large dose). Is it this more persisting stimulation you refer to as 'interesting' adrenergic effects?

Refluxer said:
As a side note that may have escaped some readers, this is a big reason why nitrogen is so abundant in compounds with pharmacological action.

Aha. I haven't thought of this before.
 
kaskelot said:
The mephedrone-euphoria wears of quite quickly, but the methylphenidate-like stimulation carries on for an hour or two (or a bit more if taking a large dose). Is it this more persisting stimulation you refer to as 'interesting' adrenergic effects?

I was more thinking about its effects on BP and heart rate I think a few of these type of betahydroxy amines have been looked as sympathomimetic drugs.

I think correlating subjective effects with speculative mechanisms in the absence of hard data is a road to nowhere. but it is entertaining to watch.
 
vecktor said:
I was more thinking about its effects on BP and heart rate I think a few of these type of betahydroxy amines have been looked as sympathomimetic drugs.

I think correlating subjective effects with speculative mechanisms in the absence of hard data is a road to nowhere. but it is entertaining to watch.

Mephedrone does indeed have quite alarming effects on blood pressure and heart rate, in me and according to a large quantity of anecdotal reports on swedish drugforums.

This is the main reason why I did not keep on doing it from time to time despite easy acquirance, it is a very short euphoric rush followed by possibly very anxiogenic stimulation with these 'interesting' adrenergic effects. Also, I'm a bit weary about toxic metabolites and the serious adverse effects overuse seems to cause according to same anecdotal material as above. Some people have trouble abstaining from redosing, as well.

Hard data is required to make definite statements, of course I realise that. But speculation can produce at least some ideas about how cautious one needs to be, which in turn can keep people from doing really stupid things, that kind of people who will take the substance regardless of warnings about use of so called RC's but may be convinced to keep their doses low with some well-educated guessing about dangers as a measure of safety.

My english isn't very good, I hope it works well enough to be intelligible though.
 
In my own (subjective) experience, the euphoria from mephedrone (plain one, no 4-methyl) was similar with methylphenidate induced euphoria, considering duration and intensity.
But with the mephedrone, effects on heart rate were indeed noticable but IMO nothing to worry about if one keeps the dose low and redose only 2-3 times maximum. When taking more it gets annoying...

Murphy
 
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