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selective beta-endorphine reuptake inhibitor?

sekio said:
how so?
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I don't know the exact pharmacology of it. But when Nicotine binds to the Nicotinic Acetylcholine receptors - the synopsis releases Acetylcholine. This heightened Cholinergic activity stimulates the release of Dopamine as well as Serotonin, Vasopressin, Oxytocin, Epinephrine, Norepinephrine, Etc... and through this complex process it also stimulates the release of Beta-Endorphin.

Again, I'm unsure of the exact pharmacology -but here is a paste from the Mayo Clinic's website.

Ann Meeker-O'Connell Neurologist MayoClinic said:
Like acetylcholine, nicotine leads to a burst of receptor activity. However, unlike acetylcholine, nicotine is not regulated by your body. While neurons typically release small amounts of acetylcholine in a regulated manner, nicotine activates cholinergic neurons (which mainly use acetylcholine to communicate to other neurons) in many different regions throughout your brain simultaneously. This stimulation leads to:

Increased release of acetylcholine from the neurons, leading to heightened activity in cholinergic pathways throughout your brain. This cholinergic activity calls your body and brain to action, and this is the wake-up call that many smokers use to re-energize themselves throughout the day. Through these pathways, nicotine improves your reaction time and your ability to pay attention, making you feel like you can work better.

Stimulation of cholinergic neurons promotes the release of the neurotransmitter dopamine in the reward pathways of your brain. This neural circuitry is supposed to reinforce behaviors that are essential to your survival, like eating when you're hungry. Stimulating neurons in these areas of the brain brings on pleasant, happy feelings that encourage you to do these things again and again. When drugs like cocaine or nicotine activate the reward pathways, it reinforces your desire to use them again because you feel so at peace and happy afterwards.

Release of glutamate, a neurotransmitter involved in learning and memory - Glutamate enhances the connections between sets of neurons. These stronger connections may be the physical basis of what we know as memory. When you use nicotine, glutamate may create a memory loop of the good feelings you get and further drive the desire to use nicotine.

Nicotine also increases the level of other neurotransmitters and chemicals that modulate how your brain works. For example, your brain makes more endorphins in response to nicotine. Endorphins are small proteins that are often called the body's natural pain killer. It turns out that the chemical structure of endorphins is very similar to that of heavy-duty synthetic painkillers like morphine. Endorphins can lead to feelings of euphoria also. If you're familiar with the runner's high that kicks in during a rigorous race, you've experienced the "endorphin rush." This outpouring of chemicals gives you a mental edge to finish the race while temporarily masking the nagging pains you might otherwise feel.
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The Mayonaise Clinic said:
For example, your brain makes more endorphins in response to nicotine.
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Since this doesn't even reference primary studies, the relevant mechanism is pretty ambiguous. This study demonstrates that nicotinic acetylcholinergic agonism should induce endorphin release: http://www.sciencedirect.com/science/article/pii/S002432059700444X (I'm out of academia and thus unable to penetrate paywalls :().

However, we don't know to what degree this effect is downstream, nor can we determine whether it's truly behaviorally relevant (at least from the study linked).

ebola
 
ebola? said:
Since this doesn't even reference primary studies, the relevant mechanism is pretty ambiguous. This study demonstrates that nicotinic acetylcholinergic agonism should induce endorphin release: http://www.sciencedirect.com/science/article/pii/S002432059700444X (I'm out of academia and thus unable to penetrate paywalls :().

However, we don't know to what degree this effect is downstream, nor can we determine whether it's truly behaviorally relevant (at least from the study linked).

ebola
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I agree I also thought that was poorly phrased - but keep in mind - they're trying to have the article make sense to everyone - not just those with a degree in pharmacology.

So what you're saying is I'm right - correct? That what I got out of the article you pasted.
 
I mean, if anecdotal evidence means anything, plenty of heroin addicts "nod out" more when using tobacco. I know that I myself (without opiates) get a distinct "noddy" feeling when using tobacco; I guess it could be due to GABAergic activity. Wait a minute, this is ADD, fuck anecdotes!

I think its fairly well established that nicotinic acetylcholline agonism leads to beta-endorphin release though...

http://www.sciencedirect.com/science/article/pii/S002432059700444X
http://www.sciencedirect.com/science/article/pii/0091305785903971
 
I think I read that endorphin uptake is adsorption mediated, meaning that it binds to anionic sites on the cell surface. To do this first an albumin complex may be formed that has cationic functions. I don't know the rest of the transcytosis mechanism but apparently a transporter is not involved (otherwise it would be called transporter mediated diffusion).

Try googling some of that to see if you can confirm for yourself. I arrived at this because of a recent kambo thread in ADD.

If what I said is correct, there would be no transporter to inhibit and I would really recommend against tweaking albumin complexing or something like that, to interfere with polar interactions / adsorption - because it would probably not be selective and it sounds like a good way to cause a syndrome nobody ever had before. D:
 
nigella sativa really FEELS like it makes me more sensitive to endorphins... i believe thymoquinone(the active chemical) is mainly a delta opiod agonist. it definitely makes opiates stronger.

point being it may be worthwhile to start looking into delta opiod agonists , as increasing sensitivity would be an interesting way to get beta-endorphins to do more for less neurotransmitter. i get huge boosts at the gym from thymoquinone but im not sure it completely endorphin mediated- thymoquinone has some NO modulating effects . it may be possible the delta opiod agonist is balancing out some respiratory depression as well...

if anyone is familiar with the pharmacology of tianpetine, lowering the amount of needed serotonin to trigger an impulse - would lowering the amount of endorphin needed to trigger a response be a viable mechanism of action? granted the pharmacology of tianeptine is not too well understood but I don't know of anything with similar pharmacology
 
You need more then 60% reuptake of most monoamines for significant effects, what your trying to do prob wont do more then getting a kiss from mommy.
 
You need more then 60% reuptake of most monoamines for significant effects,
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Do you mean reuptake inhibition? And how did you arrive at this figure? And why would opioid reuptake be analogous (given the importance of the mechanism Solipsis outlined, and that opioid reuptake is poorly understood at this point (other studies suggest that there are indeed endorphin transporters))?

what your trying to do prob wont do more then getting a kiss from mommy.
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Depending on the situation, this can be pretty potent in effect if brief in duration. :P

ebola
 
You guys might find my post on Dilantin/Phenytoin interesting....it is said to release endorphins....I take dilantin and am a subjective witness to the effect. Your Welcome.
 
ground000 said:
You guys might find my post on Dilantin/Phenytoin interesting....it is said to release endorphins....I take dilantin and am a subjective witness to the effect. Your Welcome.
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There are many drugs that indirectly release endorphins. Nicotine does, so do amphetamines, however, what were refering to is a substance that would directly release endorphins and/or stops its reuptake.
 
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