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Norepinephrine releaser

Curiously, though, it seems to produce more "liking" than other NE releasers. However, almost all of the other bk-amphetamines based on other recreational drugs 'appear' to exert great direct adrenergic agonism (at least methcathinone does for sure).
 
I guess that the N-ethyl group in ethcathinone makes it unsuitable for adrenaline receptor affinity. Though it will be somehow metabolized into cathinone making it a powerful DA and Adrenaline releaser.

The statistics are pretty obvious, beta ketones, alcohols and ethers seems to stimulate E and NE receptors way more than other simple amphetamines. Not so unexpected anyway judging on the beta polarity.
 
ebola? said:
Do we have a drug that presents a high selectivity for NE release but with little to no adrenergic activity?

ebola
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Isn't that in the realms of the oxymoron?


I guess that the N-ethyl group in ethcathinone makes it unsuitable for adrenaline receptor affinity. Though it will be somehow metabolized into cathinone making it a powerful DA and Adrenaline releaser.
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What's the primary metabolite of ethcathinone (considering ethcathinone is the primary metabolite of diethylpropion)?
 
seep said:
Limpet chicken, the side effects you experienced from mirtazapine are rare.
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I'm the only person I know of to become Suicidal from Mirtazapine :\
It's not even listed as a side effect on the info leaflet, so I had to fill out one of those yellow cards that you state the side effect on.
From day one I was having Suicidal Ideation and stopped after 4 days of use I think it was. As soon as I stopped it the Suicidal Ideation stopped also.

I'm curious if anyone else has had this effect, as I've heard that it's one of the best Antidepressants around for a great deal of people.
 
The Monkey Mantra said:
nM = nanoMolar. Moles to the negative ninth. It's a concentration of the drug at which it's effective in 50 % of the population, hence EC50.
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Thought it was some direct measure of neurotransmitter flow out of the neuron, like concentration at which 50% of some maximum outflow is achieved? (Could be wrong; I'm just an amateur)
 
Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase. It is released from the adrenal medulla into the blood as a hormone, and is also a neurotransmitter in the central nervous system and sympathetic nervous system where it is released from noradrenergic neurons. The actions of norepinephrine are carried out via the binding to adrenergic receptors.

Staying on topic...To perform its functions, norepinephrine needs to be released from synaptic vesicles. Many substances modulate this release, some inhibiting it and some stimulating it.
For instance, there are inhibitory α2 adrenergic receptors presynaptically, that gives negative feedback on release by homotropic modulation.
 
Thanks. So what we'd want to minimize is direct agonism at E/NE receptors and then maximize selectivity for CNS over PNS effects (unless you're in to jittery nightmares).
 
I have two question - first why then NE said to be psychoactive, while epiniphrine is not?
And about negative feedback - does it mean that more we get NE released from vesicles - the less will be released on another releaser hit ?
missingno said:
Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase. It is released from the adrenal medulla into the blood as a hormone, and is also a neurotransmitter in the central nervous system and sympathetic nervous system where it is released from noradrenergic neurons. The actions of norepinephrine are carried out via the binding to adrenergic receptors.

Staying on topic...To perform its functions, norepinephrine needs to be released from synaptic vesicles. Many substances modulate this release, some inhibiting it and some stimulating it.
For instance, there are inhibitory α2 adrenergic receptors presynaptically, that gives negative feedback on release by homotropic modulation.
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d-Ephedrine and ethcathinone come to mind... Someone should buy some o-Acetyl ephedrine and see if it's any better of a stimulant than regular ol' ephedrine.

An old post:
O & N-acetyl ephedrine interchange quite easily depeding upon the pH of the solution they're in (<7 ie acidic results in O-acetylephedrine where >7 ie alkaline favours the amide formation). I came across this many, many years ago and I think it was an OK stimulant - I don't have any 'real horror show' memories of it as I do of ephedrine (and I mean many - lots of drug fillee waters have flowed under the bridge since then!) with not too much of the hideous ephedrine feel - think that's to do with the dose required - 20mg - not producing enough ephedrine metabolite to bugger it all up.

Having an acetyloxy group on the benzylic carbon improves BBB penetration & prevents direct action on receptors that ephedrine has (benzylic OH groups seem to increase noradrenergic activity in preference to dopaminergic - esterify it and you push it more towards the dopamine activity).

If I remember it's not that stable - my sample stunk of acetic acid after a few weeks without the benefit of an airtight contaner including dessicant
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interesting, nuke.

first why then NE said to be psychoactive, while epiniphrine is not?
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IIRC, adrenalin doesn't cross the BBB.

And about negative feedback - does it mean that more we get NE released from vesicles - the less will be released on another releaser hit ?
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If I understand the wiki article on allosteric modulation (;)), not quite, at least from what you quote alone. Rather, NE's agonism at alpha-2 adrenal receptors induces changes in the presynaptic cell's adrenal receptors that reduce subsequent binding of NE. This would also effect the efficacy of releasers w/o affecting the quantity of NE released.
 
I've been taking Effexor, which is an odd structure of a chem to say the least.

It's pretty sweet as far as AD effects are concerned, and the norephinrine re-uptake inhibition characteristics do a sweet job on my adult ADD as well.

Also I've heard once I surpass 225mg it starts working on dopamine as well (I'm currently taking 75mg). Interesting chemical to say the least.
 
thouart_that said:
I've been taking Effexor, which is an odd structure of a chem to say the least.

It's pretty sweet as far as AD effects are concerned, and the norephinrine re-uptake inhibition characteristics do a sweet job on my adult ADD as well.

Also I've heard once I surpass 225mg it starts working on dopamine as well (I'm currently taking 75mg). Interesting chemical to say the least.
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yes with an interesting withdrawl
 
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