469 replies to this topic

[Billybear185]

Quick question... If you really did carry out an objective study of piracetam, how is it that you posted first about the research you were going to do, then 30 minutes later your results from this experiment were done.

Your first post was a 2:31 PM on February 15 2012 and the second post was at 2:52 PM on February 14 2012. Hmmm... that was some pretty fast research...

[Baten]

I took my daily stack which includes 6g morning dose of piracetam and went out to school, on my way back I noticed, OUT OF NOWHERE, the saturation effect mentioned so many times before.
I haven't change a thing in my exercise or stack habits nor diet (don't take glutamic acid), so it's pretty random, but right now all colors pop out, it's pretty cool albeit useless.

Edited by Baten, 26 April 2012 - 02:18 PM.

[Eric S Suyoto]

finally i found this, who talking about piracetam...

i have some question if i drink piracetam 800mg is it oke if i drink 2 pill in a day??? coz sometime i feel the effect but sometime i don't feel it

sorry for my bad English :D

[SuperjackDid_]

finally i found this, who talking about piracetam...

i have some question if i drink piracetam 800mg is it oke if i drink 2 pill in a day??? coz sometime i feel the effect but sometime i don't feel it

sorry for my bad English :D

You need stable balance of calcium and glutamate in the brain .

[camarito]

if you do not feel the effects of piracetam I have a suggestion that has not been mentioned. Just like creatine is ONLY absorbed when taken with some sugar beverage, the same applies to piracetam. try mixing 5g of piracetam with the same ammount , not weight, of sugar, and them tell me the results.

[medievil]

I took my daily stack which includes 6g morning dose of piracetam and went out to school, on my way back I noticed, OUT OF NOWHERE, the saturation effect mentioned so many times before.
I haven't change a thing in my exercise or stack habits nor diet (don't take glutamic acid), so it's pretty random, but right now all colors pop out, it's pretty cool albeit useless.

Hmm yeah its pretty strange when piracetam starts working; like a stable platform in the background it feels (saturation/colors) indeed have some relevance to prescribing how it feels; strange and hard to describe.

[Cephalon]

Who ever this guy is, the Calcium thing works for me - I'm not sure about it though.
It definately makes it different. Vision seems improved, overall perception is a little shifted (I would say this is neutral).
I feel a little tired and I have a wired sensation that feels like little ants were crawling over my legs. (hope this is not what's prior to a stroke or seizure )
I never took a calcium supplement as far as I can remember - my diet is pretty low in calcium as well.
I will give it some further goes, but actually I'm a pretty good responder already. Piracetam never made me sleepy which is strange.
Even a big cup of strong black coffee does not really pick me up (which is no problem because since it's so hot today I'm comfortable hanging out ...)
Won't try the Glutamate though - I have not been avoiding places that use this stuff, just to take it spoonwise ...

Edited by Cephalon, 24 May 2012 - 06:49 PM.

[Cephalon]

Vision is sustainably enhanced - effects from 1200mg Piracetam with 400mg Calcium last for several hours now - Life is in high definition now :-) don't notice much else except some good mood. Will try this again tomorrow morning ; lets see if this is reproducible!

Edit: whoohoo just saw a construction worker in an bright orange jumpsuite :-) wow was that bright!

Edit2: anyone knows if isochroma has a preference for Asian foods and dairy products? :-)

Edited by Cephalon, 24 May 2012 - 08:36 PM.

[Cephalon]

Unfortunately the effects were not reproductible. Piracetam still worked fine as usual though.

[SuperjackDid_]

No one interest in this thread anymore ,by induce in excitotoxin when combine with MSG or glutamic with PI?

My diet contain a lot of MSG so i lacked calcium ,but effect can start by without Piracetam when MSG/Calcium in balance state .

So i have partial effect simply by MSG supplement and additional Calcium if i need for vision improvement .
Problem is long-term user Piracetam cause over-stimulation and further put more Piracetam seem get negative effect opposite to supplement MSG a lone ,um.


But i still need full Piracetam effect ,induce by larger Piracetam dose ,anyone post more experience base ?

(Sorry for grammar ,and brain damaged symptom )

I try to avoid further damage to maintain my life .

[Sun]

i've read in this thread that piracetam has something to do wih calcium depletion...
i was wondering if it would affect the recovery from a bad fracture, or it's a completely other thing and i can take my piracetam doses with no worries, thanks guys

[CIMN]

I took my daily stack which includes 6g morning dose of piracetam and went out to school, on my way back I noticed, OUT OF NOWHERE, the saturation effect mentioned so many times before.
I haven't change a thing in my exercise or stack habits nor diet (don't take glutamic acid), so it's pretty random, but right now all colors pop out, it's pretty cool albeit useless.

Hmm yeah its pretty strange when piracetam starts working; like a stable platform in the background it feels (saturation/colors) indeed have some relevance to prescribing how it feels; strange and hard to describe.

i get the same effect but from just drinking coffee/caffeine.
colors pop out, get vibrant and saturated. it might have to due somehow that these substances effect receptors in the eyes.

[SuperjackDid_]

How to lower glutmate level ?,sometime effect inhibit by too much glutamate level,i have experiment a lot of glutamate /calcium ratio ,now i known how much dose each ,but sometime glutamate just too much .

Now i get all benefit Piracetam can provided ,low or too high glutamate seem inhibit so many effect such as hearing,concentration,creative ,calcium most respond to vision improvement,sometime improve hearing .

[FelixTheCat]

First a little bit of background:

25 year old Male

175 lbs. ~80 kg

Vegan for the past 2 months.

I've been taking Piracetam for the past 6 months off and on. (800 mg tablets of Nootropil) with little to no effect. Typically I would take 3 tablets in the morning (2.4 g) and not feel much.

I spent a couple days reading through this thread and the one associated with it to gather some information that may help with the potential of Piracetam as I've heard so much positive information on this subject.

When I heard the idea of a glutamic acid deficiency I went into my kitchen to see what I had that might solve this problem, here is what I found in my roommates whey protein blend.

(I apologize to all vegans out there, I broke the code... My vegan powers will be stripped soon I know this)

The whey protein blend (I will leave the name out, I don't want to appear as a peddler),

Here is what is contained in one 38g scoop.
140 calories
2g fat
1 g saturated fat
50 mg cholesterol
8g carbohydrate
<1 g dietary fiber
2 g sugar
26 g protein
64 mg calcium
0.5 mg iron
62 mg phosphorus
18 mg magnesium
0.09 mg zinc
0.05 mg copper
100 mg sodium
190 mg potassium

336 mg histidine
1,118 mg isoleucine
1,914 mg leucine
1,566 lysine
407 mg methionine
623 mg phenylalanine
1,215 threonine
314 mg tryptophan
1,091 mg valine
869 mg alanine
449 mg arginine
2,099 apartic acid
408 cysteine
2,867 glutamic acid (the ingredient I was looking for)
351 mg glycine
1,108 mg proline
921 mg serine
403 mg tyrosine


Consumption for the day. I had approximately 24 oz. of coffee 3-4 hours prior to Piracetam.

Took 4.8 g (6 800 mg tablets) and washed down with a mixture of 1 38 gram scoop of whey protein mixed with 8 oz of water.

The following ensued. at first tightness in the temples/eyes. This lasted for about 20 minutes. Immediately followed by a burning sensation in the back right area of the crown of my head. This lasted approximately 15 minutes (I seriously hope I did not fry my brain in a significant way).

When this subsided I noticed a significant feeling of alertness and confidence. My eyes hurt as well, almost as if everything was "too bright".

I was unable to suffer impoliteness from anyone (I work in customer service and typically can deal with terrible CSR's), and felt an extreme need to accomplish tasks quickly.

Side note: typically I will have an idea get excited, then the idea will whither away or I will feel exhausted by the sheer act of creating it, however while dosed I felt able to continue the train of thought and create plans for its achievement.

At about 3 hours I felt a headache on the left side running almost as a straight line through the top of my head. I took 400 mg of Choline in the form of lecithin and within 10 minutes the headache went away.

So... I cannot definitively say that the experience was the work of the glutamic acid, or the Piracetam being that my body was heavily deficient in all of those amino acids. I can however say that this experience sounds very similar to the experience of those I've read about utilizing Piracetam. So my belief is that my body was deficient in "something" that was necessary for Piracetam to fully take effect.

Subject 2:

My mother in law is weaning herself off of Zoloft, she found my Noots and grabbed an Intellectol (Vinpocetine). I recommended that she take some Piracetam as I believed that would help with the transition period.

She weighs 150 lbs, approximately 67 kg. I gave her 4.8 g the same that I took yesterday.

Her experience is as follows,. She stated that she took a nap for an hour and a half, and afterwards stated she could "smell testosterone in the air" she was very flirtatious (not out of character for her) but had a goal in mind of "making friends". Colors were enhanced, as well as mood elevation, increased taste sensations and sound acuity.


This leads me to believe that the correct dosage is closer to 1g/10kg.

I will be testing tomorrow with no adulterants and reporting back.

FYI to everyone I am no longer a Vegan (I missed eating chicken, and beef) and I feel better,

[FelixTheCat]

So. Yesterday I attempted the 8 g of Piracetam... didn't feel a thing. Too bad, was hoping I had caught onto something.

[Revolutionary]

I take 3g of choline bitartrate 3x a day and I have no side effects so far. However I notice I am lacking calcium in my diet, I will supplement calcium tabs and glutamine and report back.

That is an excessive amount of CHOLINE, and unecessary for ensuring that PIRACETAM works properly. The vast majority of individuals taking that dosage of CHOLINE would experience SIDE EFFECTS; if you don't, then you are very lucky

However, you should consider significantly reducing your CHOLINE dosage to the minimum dosage that prevents PIRACETAM induced CHOLINE DEIFICENCY SYMPTOMS from occurring IF or WHEN you start to notice that you start to experience any of the following EXCESS CHOLINE related SIDE EFFECTS:

DEPRESSION, NAUSEA, HEADACHE, STOMACH UPSET, DIARRHEA, FISHY BODY ODOUR, INCREASED BODY TEMPERATURE, INSOMNIA, SLEEP DISTURBANCES, GASTROINTESTINAL DISTURBANCES.

Thank you for pointing this out. I was on the verge of consuming too much choline that past couple of weeks, been taking 2+g 2x a day... Gonna cut back to 600mg 2x a day.

[stablemind]

If someone were to experience hypomania while on low doses of Piracetam, is this effect amplified if the user takes Pramiracetam?

[SuperjackDid_]

If someone were to experience hypomania while on low doses of Piracetam, is this effect amplified if the user takes Pramiracetam?

I think it should dumped down , because of Pramiracetam seem to dump emotion down and you will get less high ,and focus to work or do someting motivate you instead .

Worth a try ,it most my fault that i usually take Piracetam individual ,key might come from racetam combination .

What dose give you hypomania effect ?

[stablemind]

If someone were to experience hypomania while on low doses of Piracetam, is this effect amplified if the user takes Pramiracetam?

I think it should dumped down , because of Pramiracetam seem to dump emotion down and you will get less high ,and focus to work or do someting motivate you instead .

Worth a try ,it most my fault that i usually take Piracetam individual ,key might come from racetam combination .

What dose give you hypomania effect ?

Are you saying Pramiracetam dulls your emotions? I've gotten hypomania on 800mg of Piracetam after a couple days of use.

[SuperjackDid_]

right ,it dull my emotion ,but it lift my motivation do to so many-thing .

for hypo-mania i thin this thread worth while ,for choline deficiency symptom

http://www.longecity...iracetam-mania/


add more choline to avoid hypo-mania to occur .

[SuperjackDid_]

Piracetam-induced changes in the functional activity of neurons as a possible mechanism for the effects of nootropic agents.

Verbnyi YaI, Derzhiruk LP, Mogilevskii AYa.

Source

Physical-Technical Low Temperature Institute, National Academy of Sciences of Ukraine, Khar'kov.

Abstract

Studies were carried out on the effects of piracetam (4-20 mM) on the electrical activity of identified neurons in the isolated central nervous system of the pond snail in conditions of single-electrode intracellular stimulation and recording. Piracetam-induced changes were seen in 60-70% of the neurons studied. Different parameters showed different sensitivities to piracetam: the most frequent changes were in the action potential generation threshold, the slope and shape of the steady-state voltage-current characteristics of neuron membranes, and the appearance of piracetam-induced transmembrane ion currents. Nifedipine and cadmium ions, both of which are calcium channel blockers, generally reversed or weakened the effects of piracetam on the changes seen in test cells. This indicates that the effects of piracetam result from its action on calcium channels; selective changes in calcium channels may determine which piracetam-induced effects appear at the cellular level. It is hypothesized that the piracetam-sensitive cellular plasticity mechanisms may make a significant contribution to its nootropic action at the behavioral level.

[SuperjackDid_]

More

Piracetam and other structurally related nootropics

• Alex Haahr Gouliaev^a,
• Alexander Senning^{, b}

• ^a Department of Chemistry, Aarhus University, Langelandsgade 140, DK-8000 Aarhus C, Denmark
• ^b Department of Chemistry and Chemical Engineering, The Engineering Academy of Denmark, Building 376, DK-2800 Lyngby, Denmark

Abstract

Nearly three decades have now passed since the discovery of the piracetam-like nootropics, compounds which exhibit cognition-enhancing properties, but for which no commonly accepted mechanism of action has been established. This review covers clinical, pharmacokinetic, biochemical and behavioural results presented in the literature from 1965 through 1992 (407 references) of piracetam, oxiracetam, pramiracetam, etiracetam, nefiracetam, aniracetam and rolziracetam and their structural analogues. The piracetam-like nootropics are capable of achieving reversal of amnesia induced by e.g., scopolamine, electrocon-vulsive shock and hypoxia. Protection against barbiturate intoxication is observed and some benefit in clinical studies with patients suffering from mild to moderate degrees of dementia has been demonstrated. No affinity for the α₁-, α₂-, β-, muscarinic, 5-hydroxytryptamine-, dopamine, adenosine-A₁, μ-opiate, γ-aminobutyric acid (GABA) (except for nefiracetam (GABA_A)), benzodiazepine and glutamate receptors has been found. The racetams possess a very low toxicity and lack serious side effects. Increased turnover of different neurotransmitters has been observed as well as other biochemical findings e.g., inhibition of enzymes such as prolylendopeptidase. So far, no generally accepted mechanism of action has, however, emerged. We believe that the effect of the racetams is due to a potentiation of already present neurotransmission and that much evidence points in the direction of a modulated ion flux by e.g., potentiated calcium influx through non-l-type voltage-dependent calcium channels, potentiated sodium influx through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor gated channels or voltage-dependent channels or decreases in potassium efflux. Effects on carrier mediated ion transport are also possible.

[Isochroma]

Back again after some years. Was getting too hot.

I'm on the Piracetam/MSG protocol. Today is day 13 on it. Dose is 5g PIR / 2.5g MSG x 6 per day.

Totals are: PIR: 30g/day, MSG: 15g/day.

I also take 1:1 Ca:Mg totalling 1g (elemental) of each per day.

This post is also to bring forth evidentiary material in support of the glutamate/calcium hypothesis.

Below is pasted the email I sent a few days ago to my Piracetam supplier telling them the good news. It is the most cogent and sensical collation of materials in support of the hypothesis that I have been able to generate so far. Below begins the material:

--------------

A week ago I found on a forum that a new study finds that taking Monosodium Glutamate (MSG) can make Piracetam work much better! Even for people who lost the effects over time.

MSG

I bought the MSG above (Accent brand) from a local store: 128g for $4.59

So the last Piracetam batch you shipped to me, I am testing it right now with MSG!

I take 2.5g MSG + 5g Piracetam x 6 per day (total = 30g/day Piracetam, 15g/day MSG).

Piracetam causes the brain to slowly decrease its Glutamate so it has to be replenished by supplementation.

It's amazing so far, the colors are 80% as saturated as Oxiracetam without the diarrhea and I have no tiredness yet. I know that Piracetam is not strong enough to prevent the brain tiredness but it takes 2-5 weeks of Piracetam for the tiredness to begin to appear so I'm not sure if the MSG is working or not yet.

I have the science papers on it, it's complicated. There are 3 molecular pumps inside the brain for glutamate. Two are sodium-dependent efflux (they pump Glutamate out of the brain), and the other one is an influx transporter and was recently discovered and it is Calcium dependent and pumps glutamate INTO the brain!

The forum poster said he tested people with Piracetam + Glutamate + Calcium and he said it works. Two other people on the forum tried the MSG and said it works too.

I can send you the links and references if you are interested. Below are the most important studies which show why it works:

ATP stimulates calcium-dependent glutamate release from cultured astrocytes

Calcium ions induce glutamate transport into rat brain membrane vesicles in the absence of sodium and chloride. Evidence for a novel uptake site

Glutamate transport and not glutamate receptor binding is stimulated by gangliosides in a Ca2+-dependent manner in rat brain synaptic plasma membranes

"The observed increase in glutamate binding was not due to a change in the affinity of the binding sites, but to a change in the number of binding sites, and it was absolutely dependent on the presence of Ca2+."

[Piracetam causes increase of glutamate receptors (binding sites).]

BUT! This is the most amazing study, it finds a direct connection:

The glutamate transport inhibitor L-trans-pyrrolidine-2,4-dicarboxylate indirectly evokes NMDA receptor mediated neurotoxicity in rat cortical cultures

L-trans-pyrrolidine-2,4-dicarboxylate (PDC)

Abstract

"Because of the well-documented importance of glutamate uptake in protecting neurons against glutamate toxicity, we were interested in testing the effects of L-trans-pyrrolidine-2,4-dicarboxylate (PDC) on rat cortical cultures. This compound is a substrate for glutamate transporters and is a potent glutamate transport inhibitor that does not interact significantly with glutamate receptors. Using a 30 min exposure, and assessing neuronal survival after 20-24 h, PDC was neurotoxic in conventional astrocyte-rich cortical cultures, with an EC50 in these cultures of 320 +/- 157 microM. In astrocyte-poor cultures, an EC50 for PDC of 50 +/- 5 microM was determined. The neurotoxicity of PDC in both astrocyte-rich and astrocyte-poor cultures was blocked by the NMDA antagonist MK-801, but not by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). We tested the possibility that the neurotoxicity of PDC might be due to release of excitatory amino acids using several approaches. After pre-loading cells with the non-metabolizable analogue of glutamate, [3H]-D-aspartate, first we demonstrated that PDC caused significant efflux of [3H]-D-aspartate. This effect of PDC was dependent upon extracellular sodium. In contrast with glutamate neurotoxicity, PDC neurotoxicity was inhibited by removal of extracellular sodium. In the presence of 1 mM PDC, sodium caused neurotoxicity with an EC50 of 18 +/- 7.6 mM. Tetrodotoxin had no effect on either PDC neurotoxicity or on PDC-evoked [3H]-D-aspartate release. PDC-evoked release of [3H]-D-aspartate was demonstrable in astrocyte cultures with no neurons present. PDC also evoked release of endogenous glutamate. Finally, the neurotoxicity of PDC was blocked by coincubation with glutamate-pyruvate transaminase plus pyruvate to degrade extracellular glutamate. These results demonstrate the neurotoxicity of PDC, and suggest that the mechanism of this toxicity is the glutamate transporter-dependent accumulation of glutamate in the extracellular space."

And finally the most important study! Rememer that Piracetam is almost the same as Pyroglutamate:

(Left: Pyroglutamate; Right: Piracetam)

Pyroglutamate stimulates Na+ -dependent glutamate transport across the blood-brain barrier

"Regulation of Na(+)-dependent glutamate transport was studied in isolated luminal and abluminal plasma membranes derived from the bovine blood-brain barrier. Abluminal membranes have Na(+)-dependent glutamate transporters while luminal membranes have facilitative transporters. This organization allows glutamate to be actively removed from brain. gamma-Glutamyl transpeptidase, the first enzyme of the gamma-glutamyl cycle (GGC), is on the luminal membrane. Pyroglutamate (oxoproline), an intracellular product of GGC, stimulated Na(+)-dependent transport of glutamate by 46%, whereas facilitative glutamate uptake in luminal membranes was inhibited. This relationship between GGC and glutamate transporters may be part of a regulatory mechanism that accelerates glutamate removal from brain."

Remember that Na+ transporters REMOVE Glutamate from the brain. So Pyroglutamate causes the two Na+ transporters to pump more Glutamate out of the brain and also inhibits Glutamate uptake in luminal membranes. Eventually this produces a deficiency of Glutamate in the brain. Piracetam might cause the same effect as Pyroglutamate because the molecules are so similar.

So the idea is to eat large amounts of Glutamate (as MSG) to correct the deficiency.

Edited by Isochroma-Reborn, 27 November 2012 - 04:38 AM.

[1thoughtMaze1]

Back again after some years. Was getting too hot.

I'm on the Piracetam/MSG protocol. Today is day 13 on it. Dose is 5g PIR / 2.5g MSG x 6 per day.

Totals are: PIR: 30g/day, MSG: 15g/day.

I also take 1:1 Ca:Mg totalling 1g (elemental) of each per day.

This post is also to bring forth evidentiary material in support of the glutamate/calcium hypothesis.

Below is pasted the email I sent a few days ago to my Piracetam supplier telling them the good news. It is the most cogent and sensical collation of materials in support of the hypothesis that I have been able to generate so far. Below begins the material:

--------------

A week ago I found on a forum that a new study finds that taking Monosodium Glutamate (MSG) can make Piracetam work much better! Even for people who lost the effects over time.

MSG

I bought the MSG above (Accent brand) from a local store: 128g for $4.59

So the last Piracetam batch you shipped to me, I am testing it right now with MSG!

I take 2.5g MSG + 5g Piracetam x 6 per day (total = 30g/day Piracetam, 15g/day MSG).

Piracetam causes the brain to slowly decrease its Glutamate so it has to be replenished by supplementation.

It's amazing so far, the colors are 80% as saturated as Oxiracetam without the diarrhea and I have no tiredness yet. I know that Piracetam is not strong enough to prevent the brain tiredness but it takes 2-5 weeks of Piracetam for the tiredness to begin to appear so I'm not sure if the MSG is working or not yet.

I have the science papers on it, it's complicated. There are 3 molecular pumps inside the brain for glutamate. Two are sodium-dependent efflux (they pump Glutamate out of the brain), and the other one is an influx transporter and was recently discovered and it is Calcium dependent and pumps glutamate INTO the brain!

The forum poster said he tested people with Piracetam + Glutamate + Calcium and he said it works. Two other people on the forum tried the MSG and said it works too.

I can send you the links and references if you are interested. Below are the most important studies which show why it works:

ATP stimulates calcium-dependent glutamate release from cultured astrocytes

Calcium ions induce glutamate transport into rat brain membrane vesicles in the absence of sodium and chloride. Evidence for a novel uptake site

Glutamate transport and not glutamate receptor binding is stimulated by gangliosides in a Ca2+-dependent manner in rat brain synaptic plasma membranes

"The observed increase in glutamate binding was not due to a change in the affinity of the binding sites, but to a change in the number of binding sites, and it was absolutely dependent on the presence of Ca2+."

[Piracetam causes increase of glutamate receptors (binding sites).]

BUT! This is the most amazing study, it finds a direct connection:

The glutamate transport inhibitor L-trans-pyrrolidine-2,4-dicarboxylate indirectly evokes NMDA receptor mediated neurotoxicity in rat cortical cultures

L-trans-pyrrolidine-2,4-dicarboxylate (PDC)

Abstract

"Because of the well-documented importance of glutamate uptake in protecting neurons against glutamate toxicity, we were interested in testing the effects of L-trans-pyrrolidine-2,4-dicarboxylate (PDC) on rat cortical cultures. This compound is a substrate for glutamate transporters and is a potent glutamate transport inhibitor that does not interact significantly with glutamate receptors. Using a 30 min exposure, and assessing neuronal survival after 20-24 h, PDC was neurotoxic in conventional astrocyte-rich cortical cultures, with an EC50 in these cultures of 320 +/- 157 microM. In astrocyte-poor cultures, an EC50 for PDC of 50 +/- 5 microM was determined. The neurotoxicity of PDC in both astrocyte-rich and astrocyte-poor cultures was blocked by the NMDA antagonist MK-801, but not by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). We tested the possibility that the neurotoxicity of PDC might be due to release of excitatory amino acids using several approaches. After pre-loading cells with the non-metabolizable analogue of glutamate, [3H]-D-aspartate, first we demonstrated that PDC caused significant efflux of [3H]-D-aspartate. This effect of PDC was dependent upon extracellular sodium. In contrast with glutamate neurotoxicity, PDC neurotoxicity was inhibited by removal of extracellular sodium. In the presence of 1 mM PDC, sodium caused neurotoxicity with an EC50 of 18 +/- 7.6 mM. Tetrodotoxin had no effect on either PDC neurotoxicity or on PDC-evoked [3H]-D-aspartate release. PDC-evoked release of [3H]-D-aspartate was demonstrable in astrocyte cultures with no neurons present. PDC also evoked release of endogenous glutamate. Finally, the neurotoxicity of PDC was blocked by coincubation with glutamate-pyruvate transaminase plus pyruvate to degrade extracellular glutamate. These results demonstrate the neurotoxicity of PDC, and suggest that the mechanism of this toxicity is the glutamate transporter-dependent accumulation of glutamate in the extracellular space."

And finally the most important study! Rememer that Piracetam is almost the same as Pyroglutamate:

(Left: Pyroglutamate; Right: Piracetam)

Pyroglutamate stimulates Na+ -dependent glutamate transport across the blood-brain barrier

"Regulation of Na(+)-dependent glutamate transport was studied in isolated luminal and abluminal plasma membranes derived from the bovine blood-brain barrier. Abluminal membranes have Na(+)-dependent glutamate transporters while luminal membranes have facilitative transporters. This organization allows glutamate to be actively removed from brain. gamma-Glutamyl transpeptidase, the first enzyme of the gamma-glutamyl cycle (GGC), is on the luminal membrane. Pyroglutamate (oxoproline), an intracellular product of GGC, stimulated Na(+)-dependent transport of glutamate by 46%, whereas facilitative glutamate uptake in luminal membranes was inhibited. This relationship between GGC and glutamate transporters may be part of a regulatory mechanism that accelerates glutamate removal from brain."

Remember that Na+ transporters REMOVE Glutamate from the brain. So Pyroglutamate causes the two Na+ transporters to pump more Glutamate out of the brain and also inhibits Glutamate uptake in luminal membranes. Eventually this produces a deficiency of Glutamate in the brain. Piracetam might cause the same effect as Pyroglutamate because the molecules are so similar.

[font=Arial]So the idea is to eat large amounts of Glutamate (as MSG) to corre

Dunce

Edited by 1thoughtMaze1, 27 November 2012 - 05:30 AM.

[Isochroma]

Pyroglutamate is the key to the brain's negative-feedback autosense loop for regulation of glutamate.

There are at least two unique sodium-dependent efflux transporters and there are also ATP (energy)-dependent efflux transporters.

One of the studies above finds that glutamate can induce brain damage under circumstances of ATP deficiency and presence of sodium and the glutamate transport inhibitor L-trans-pyrrolidine-2,4-dicarboxylate (PDC). This seems to be consistent with the natures of these two types of glutamate efflux transporters - one requiring sodium and the other needing ATP to function.

The only known influx transporter is calcium-dependent.

None of this yet touches on other questions such as the effect of glutamate supplementation on glutamate migration between pools. The brain is a net exporter but this does not mean that its glutamate content and autoregulatory mechanisms are not affected by the body glutamate pool.

Edited by Isochroma-Reborn, 27 November 2012 - 06:37 AM.

[Introspecta]

You realize the OP and this study was Fake right? And supplementing with large amounts of MSG is going to do cause nothing but problems. If anything use the lowest doses of L-glutamic acid which Is safer. I do once in awhile when I feel like I"m not getting any benefits from piracetam.

[Raza]

Fifteen grams of MSG a day is likely to go horribly wrong. Please don't.

The sodium alone... gah.

[SuperjackDid_]

Welcome back Isochroma ,keep posting.

[SuperjackDid_]

MSG do something rather than nothing ,it enhanced color contrast from 60% to 100% ,but it not make me like it anymore because i need to turn it off ,but can't .

So cool ,but it really impair my concentration,bye bye Piracetam .

I have Aniracetam more than 1KG ,hope Ani will enhance motivation and focus ,will be back.

[Isochroma]

Good morning!

Another night of amazing sleep, another night of staying up until at least 3:00am... without a trace of tiredness and in the dark.

This is day 14 exactly since starting the Piracetam (I switched from Oxiracetam / Pramiracetam). The mental fatigue and visual defocus episodes have not returned in the slightest.

It's still too early to decide in MSG's favor but I know the visual-mental desaturization curve from downswitching to Piracetam from Oxiracetam well, having gone through that transition at least four times in the last six months.

Not only is color saturation retained at a level higher than it should be (currently 80%), but there is a difference to the lamps. It's so hard to explain that manipulated photos will be necessary (later). For now, I can say that I am getting a unique visual effect which has not ever been present since summer 2008 when I started PIR. It's new.

I have experience - alone and combined - with the entire dosage range of: Piracetam, Oxiracetam, Aniracetam, Nefiracetam, Pramiracetam, Phenylpiracetam, Noopept, and Bromantane. The visual effect matches none of these nor any combination at any dosage. No other factor in my diet or other supplements has changed either.

My favorite benchmark is the high-pressure sodium streetlights. Every single night I ride my bicycle in a fixed loop around the city. Against the black sky, the spectrum of HPS bulbs is a perfect measure of the entire visual system's dynamic range. On Oxiracetam I can see in a very exaggerated way the tiny color differences between each bulb in addition to a massive increase in both color saturation and visible contrast between bulbs and black sky.

Instead of endless rows of flat-yellow lights, I see endless rows of differently-colored, reddish-orange, yellowish-orange and all the other color balances inherent in the variable runtime and electrochemistry of this type of lamp.

Oxiracetam and Aniracetam produce predictable and easily visible increases in the contrast ratio between the bulbs and black sky, increases in the color saturation of the bulbs - the high contrast maximally stresses the visual system - and edge sharpness.

Due to my severe mental fatigue due to what can only be brain damage and/or premature brain aging, I'm the ideal guinea-pig to study the restorative functions of racetams. In my case the visual saturation/sharpness exactly correlates with the decrease or elimination of excessive mental fatigue - that which is not caused by lack of sleep or other circumstances.

Tonight I will photograph the bulbs with my digicam and, using software, I will adjust the color/brightness/contrast of the images (duplicated) and upload them here to show the exact visual effect of various racetams (in my case I'm going to select for exposition: Oxiracetam, Aniracetam, Piracetam alone, and Piracetam with MSG).

In addition to this, since I was last on this board I have collected many more studies on racetams, including two which precisely measure the increase in cellular mitochondrial energy conversion from: Piracetam, Aniracetam and Oxiracetam.

Before I post the study I will tell everyone that considering only the ability to restore mitochondrial energy conversion, the power of racetams in order of declining ability is:

1. Oxiracetam
2. Aniracetam
3. Piracetam

I have verified this to be true regarding both visual color saturation and fatigue removal:

1. Oxiracetam: Color Saturation: +100%, Fatigue Removal: 90%
2. Aniracetam: Color Saturation: +90%, Fatigue Removal: 70%
3. Piracetam: Color Saturation: +20%, Sharpness: +20%, Fatigue Removal: 40-50%

It's too bad that for myself and a friend who tried it, Oxiracetam at doses >2g/day seems to inhibit proton or other pumps in the gut. This prevents the gut from pumping water out of food matter, causing diarrhea.

Because the HVS (Human Visual System) dynamically adapts to color saturation very efficiently it is hard to establish absolutes - baselines or any other measurements. So, the goal is to use very high contrast to push the HVS beyond its dynamic adaptational range.

By pushing the HVS beyond its adaptation range all the values returned become absolutes. Now, street lights at night are not totally beyond this range but they are at the edge of it. There are many other possibilities but this one is the easiest for me.

Note: I have about 1.8kg PIR and just bought another 2kg. PIR won't be enough for me and due to budget limitations I can't buy anything else for months. It's a big risk, and the investment is a measure of my own research on the glutamate synergy topic rather than blind faith in the poster's credentials or 'study'.

It is also my recommendation to others to not rely on credentials but rather do both the hard study and self-experimentation to determine the truth or falsity of the claims.

The claims are verifiable and I'm in the perfect position to find out the truth, which I am doing day by day. It's fun regardless of the outcome.

Edited by Isochroma-Reborn, 27 November 2012 - 10:09 PM.