Nicotine and Acetycholine Nootropics

Moderator's Note:

The study below demonstrates that nicotine, regardless of administration method causes Smoker's Melanosis, and it is likely that by extension, whether specifically demonstrated or not, this action will accelerate the visible signs of skin aging by a similar uneven discoloration and an increase in the number of moles which smokers and their families get. 

The long-term effect of nicotine on the oral mucosa.

 

Hi,

I just wanted to get some clarification on nicotine's role in acetycholine levels in the brain. Do they increase, decrease, or have no affect, and how would nicotine interact with choline nootropics like ALPHA GPC. Thanks in advance.

Edited by YOLF, 25 March 2017 - 01:21 AM.

They don't do anything to acetylcholine itself. There are muscarinic and nicotinic acetycholine receptors in the brain (and throughout the body). The nicotinic ones are the nootropic ones (minus a few 'bad' ones that give nicotine its side effects). Nicotine stimulates these directly, and it also causes an increase in nicotinic acetylcholine receptors. It is also a neuroprotectant and an MAO-B inhibitor and parkinson's fighter.

It's an excellent nootropic substance, one of the most powerful. Only problem is the very strong vasoconstrictive effect, which gave me terrible skin and impotence (fortunately these problems are gone now) and also ages your organs.

You really don't need to take choline if you're using nicotine (and probably you don't need it even if you're not). You really don't want to have much choline, period. Just enough that your levels are not low. Unless you're on an anticholinergic I would not supplement with it at all. At the least, check on the symptoms of too little/too much choline first. I think a lot more people have aceylcholine levels that are too high than people here would expect.

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bgwithadd, on 14-Feb 2009, 06:14 PM, said:

They don't do anything to acetylcholine itself. There are muscarinic and nicotinic acetycholine receptors in the brain (and throughout the body). The nicotinic ones are the nootropic ones (minus a few 'bad' ones that give nicotine its side effects). Nicotine stimulates these directly, and it also causes an increase in nicotinic acetylcholine receptors. It is also a neuroprotectant and an MAO-B inhibitor and parkinson's fighter.

It's an excellent nootropic substance, one of the most powerful. Only problem is the very strong vasoconstrictive effect, which gave me terrible skin and impotence (fortunately these problems are gone now) and also ages your organs.

You really don't need to take choline if you're using nicotine (and probably you don't need it even if you're not). You really don't want to have much choline, period. Just enough that your levels are not low. Unless you're on an anticholinergic I would not supplement with it at all. At the least, check on the symptoms of too little/too much choline first. I think a lot more people have aceylcholine levels that are too high than people here would expect.

Note: If you do supplment with nicotine, do so with caution. It can cause growth of blood vessels especially in the lungs. So do not use if you have activley growing tumors!

Well, if people know they have tumors growing then nootropics are the least of their worries

I'd not recommend the patchs long term now that I've tried it. I now take guanfacine and it does great for reversing those effects but I am still cautious about trying it again. Short term, I'd think it would be a much better study aid than taking adderall or ritalin, though. It provides much more drive than they do (as does wellbutrin).

What best time take Nicotine?.

I using nicotine drop right now and seem it working help me to concentrate better .

Most Nootropics not give me much benefit after so much time experimental .

I have fallback to very classical to Coffee and nicotine right now .

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I found in pubMed a very intresting article about nicotine... But I guess its not safe to take with methylphenidate...
http://www.ncbi.nlm....pubmed/16906354

Abstract


In the present work we reviewed recent advances concerning neuroprotective/neurotrophic effects of acute or chronic nicotine exposure, and the signalling pathways mediating these effects, including mechanisms implicated in nicotine addiction and nAChR desensitization. Experimental and clinical data largely indicate long-lasting effects of nicotine and nicotinic agonists that imply a neuroprotective/neurotrophic role of nAChR activation, involving mainly alpha7 and alpha4beta2 nAChR subtypes, as evidenced using selective nAChR agonists. Compounds interacting with neuronal nAChRs have the potential to be neuroprotective and treatment with nAChR agonists elicits long-lasting neurotrophic effects, e.g. improvement of cognitive performance in a variety of behavioural tests in rats, monkeys and humans. Nicotine addiction, which is mediated by interaction with nACh receptors, is believed to involve the modification of signalling cascades that modulate synaptic plasticity and gene expression. Desensitization, in addition to protecting cells from uncontrolled excitation, is recently considered as a form of signal plasticity. nAChR can generate these longe-lasting effects by elaboration of complex intracellular signals that mediate medium to long-term events crucial for neuronal maintenance, survival and regeneration. Although a comprehensive survey of the gene-based molecular mechanisms that underlie nicotine effects has yet not been performed a growing amount of data is beginning to improve our understanding of signalling mechanisms that lead to neurotrophic/neuroprotective responses. Evidence for an involvement of the fibroblast growth factor-2 gene in nAChR mechanisms mediating neuronal survival, trophism and plasticity has been obtained. However, more work is needed to establish the mechanisms involved in the effects of nicotinic receptor subtype activation from cognition-enhancing and neurotrophic effects to smoking behaviour and to determine more precisely the therapeutic objectives in potential nicotinic drug treatments of neurodegenerative diseases.