Do oxiracetam and aniracetam have the same mechanism of action on the nmda such as piracetam? Btw , I don't know what it was, visually, I felt everything was much brighter , but my brain felt foggy in my college class. I took piracetam on an empty stomach and 45 minutes later, I ingested 2 raw eggs for a choline source. Could it be that I took choline a little too late? I also think it's a good idea replenish my electrolytes since I urinate a lot, to make sure that my brain is functioning optimally.
Misc can memantine reverse methylphenidate tolerance?
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Cotcha Yankinov
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Hmmm foggyness is indeed reported by some people, that's unfortunate :/ You might try taking it with a formal source or choline, some people even get headaches if they take a racetam without choline.
Cotcha Yankinov
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I would definitely try a better source of choline like alpha gpc and see how you do, but even choline is known to cause brain fog so idk, interesting...Oxiracetam and Aniracetam are fairly different and are held in higher esteem than piracetam, I would personally try Oxiracetam if you want something stimulating, but they work in very similar ways, likely just different proportions and potencies. Aniracetam is my personal favorite.
Cotcha Yankinov
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The downregulation of acetylcholine receptors is indeed a concern although some people never have issues with this somehow, this is the primary reason I was suggesting breaks to make sure you're not getting dependent. I'm not aware of any mechanism whereby nicotinic receptors really contribute to regulation of other receptors without just influencing neuro transmission (for example, blockade of acetylcholine receptors leads to increases in dopamine flow, this is utilized in Parkinson's patients, and I imagine if chronic administration of an ampakine downregulated acetylcholine then it would result in a therapeutic increase in dopamine, while a decrease in dopamine at the start of acetylcholine stimulation would explain brain fog) but if Bobby has a source handy Id love to read it.
Oxi and ani are indeed mainly glutamate boosters, ani is almost an anti anxiety agent though while Oxi is very stimulating. Both will promote LTP, while long term DXM hasn't been shown to cause Olney's lesions or anything like that I think it is pretty clear the long term users do have deficits of learning and attention, and this is of concern. People with ADHD mainly have working memory problems, working memory is facilitated by D1 stimulation and NMDA, so I think antagonizing NMDA defeats the purpose of a racetam and an ADHD med, no matter what it does for acetylcholine receptors.
Also concentric exercise is actually pretty important, it's been shown to be vital for healthy connective tissue. I'm surprised you're not interested in grow hormone secretatogues, they are very interesting and I would use Ipamorelin + MOD GRF 1-29 myself if I wasn't afraid of needles. They can be used at a rate that doesn't desensitize growth hormone receptors easily. The main problem is actually that most of our growth hormone sits in the pituitary and decays there without ever being released, GHRH/GHRP just signals it to release before it breaks down. They have even been shown to improve one type of memory in the elderly.
Oxi and ani are indeed mainly glutamate boosters, ani is almost an anti anxiety agent though while Oxi is very stimulating. Both will promote LTP, while long term DXM hasn't been shown to cause Olney's lesions or anything like that I think it is pretty clear the long term users do have deficits of learning and attention, and this is of concern. People with ADHD mainly have working memory problems, working memory is facilitated by D1 stimulation and NMDA, so I think antagonizing NMDA defeats the purpose of a racetam and an ADHD med, no matter what it does for acetylcholine receptors.
Also concentric exercise is actually pretty important, it's been shown to be vital for healthy connective tissue. I'm surprised you're not interested in grow hormone secretatogues, they are very interesting and I would use Ipamorelin + MOD GRF 1-29 myself if I wasn't afraid of needles. They can be used at a rate that doesn't desensitize growth hormone receptors easily. The main problem is actually that most of our growth hormone sits in the pituitary and decays there without ever being released, GHRH/GHRP just signals it to release before it breaks down. They have even been shown to improve one type of memory in the elderly.
A phenomenal and informative post indeed cotcha, I still think the 1 month on piracetam and other suggested nutraceuticals with the inclusion of exercise/cardio is still the way to go about it , unless Bobby has a source proving otherwise. I just want the nmda receptors to be completely agonized before touching concerta again , otherwise I have a strong feeling that there will be flawed results. And check your inbox cotcha.
Cotcha Yankinov
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I would think that the combination of piracetam and concerta (concerta with NMDA agonism) would prove the most useful for inducing LTP.
But tolerance is a real problem, there's really no way around it. Long term administration of Concerta is a good thing for dopamine projections though, I'd suggest just sticking with it at some point and if you don't get euphoria then poop :/
But tolerance is a real problem, there's really no way around it. Long term administration of Concerta is a good thing for dopamine projections though, I'd suggest just sticking with it at some point and if you don't get euphoria then poop :/
My notion is, exercise + nmda agonism = tolerance reduced drastically if not removed? That way , not only will my nmda be agonized and sensitive , but what will also transpire , is the growth of new brain cells which facilitate in the production of mood boosting neurotransmitters as well. Then after this I thought adding concerta with piracetam will potentiate each other? I hope I am not getting lost lol
Ksa
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The brain is complicated bro. Take for example the use of dextroamphetamine to masturbate to porn. You can do it day and night until 40mg no longer does anything, but you'll be surprised to see that if you dump the porn and try to write an essay or listen to music, 5mg will be more than sufficient. Sometimes, it is not the drug itself you are developing the tolerance to, but the region of the brain that you over-use and that needs a rest.
Memantine...like I said, if you think memantine will magically remove your tolerance you're wrong. Depends what you're doing.
Cotcha Yankinov
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LTP is a facilitation of transmission that results in increased signal strength, LTP is a good thing. But idk about taking piracetam without concerta, I think taking concerta and piracetam together will produce the best results. So you might just try a good old 1 month break with cardio.
"A good old one month break with cardio" okay , when I took the three month break , my ltp got inhibited. which had me take a larger methylphenidate dosage, which , when wears off, can produce a horrible come down lol . I didn't do cardio at that time though , but then again , although cardio generates new brain cells. It doesn't agonize nmda pathways . Sorry for so many questions lol , I have the propensity to ask until I am satisfied with a definite solution. 
Cotcha Yankinov
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Okay I completely cleared my inbox. I think you're probably going to achieve the best effects from concerta after a few months of taking it with cycling on and off a racetam, but a tolerance break may or may not be worth it because you'll lose your LTP. 5-HT1A serotonin receptors are what are called auto receptors, which means that they regulate the level of serotonin release by detecting activation at 5-HT1A and then reducing the amount of serotonin released essentially. So an agonist at 5-HT1A causes inhibitory action by reducing serotonin flow. I don't think this plays much into concerta's mechanism of action though so I wouldn't worry about it. Yeah I actually just checked it, it's 5-HT1A agonism is extremely weak. I found this concerning deltafosB though https://en.wikipedia.org/wiki/File:ΔFosB_accumulation.svg
and this "At therapeutic doses, ADHD stimulants do not sufficiently activate the reward system, or the reward pathway in particular, to induce persistent ΔFosB gene expression in the D1-type medium spiny neurons of the nucleus accumbens;[78][81][88] consequently, when used medically and as directed, methylphenidate use has no capacity to cause an addiction.[78][81][88] However, when methylphenidate is used at sufficiently high recreational doses through a bioavailable route of administration (e.g., insufflation or intravenous administration), particularly for use of the drug as a euphoriant, ΔFosB accumulates in the nucleus accumbens.[78][81] Hence, like any other addictive drug, regular recreational use of methylphenidate at high doses eventually gives rise to ΔFosB overexpression in D1-type neurons which subsequently triggers a series of gene transcription-mediated signaling cascades that induce an addiction.[81][88][89][90][91]"
It seems like they imply in other places on the Wiki that deltafosB expression doesn't happen very much at dosages less than abused dosages but I imagine that deltafosB just happens a little less with therapeutic dosages and takes longer to accumulate.
and this "At therapeutic doses, ADHD stimulants do not sufficiently activate the reward system, or the reward pathway in particular, to induce persistent ΔFosB gene expression in the D1-type medium spiny neurons of the nucleus accumbens;[78][81][88] consequently, when used medically and as directed, methylphenidate use has no capacity to cause an addiction.[78][81][88] However, when methylphenidate is used at sufficiently high recreational doses through a bioavailable route of administration (e.g., insufflation or intravenous administration), particularly for use of the drug as a euphoriant, ΔFosB accumulates in the nucleus accumbens.[78][81] Hence, like any other addictive drug, regular recreational use of methylphenidate at high doses eventually gives rise to ΔFosB overexpression in D1-type neurons which subsequently triggers a series of gene transcription-mediated signaling cascades that induce an addiction.[81][88][89][90][91]"
It seems like they imply in other places on the Wiki that deltafosB expression doesn't happen very much at dosages less than abused dosages but I imagine that deltafosB just happens a little less with therapeutic dosages and takes longer to accumulate.