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Aniracetam vs. Piracetam


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#31 Rags847

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Posted 24 December 2007 - 04:43 AM

Why do you want to avoid NO (assuming you mean Nitric Oxide)?


Current research shows that NO might have benfical or detrimental effects on the brain.
I don't want to mess with it, therefore.

Here is the article on Pramiracetam and NO.

http://www.biopsychi...amiracetam.html

Systemic administration of pramiracetam increases
nitric oxide synthase activity in the cerebral cortex of the rat
by
Corasaniti MT, Paoletti AM, Palma E,
Granato T, Navarra M, Nistico G.
Faculty of Pharmacy,
University of Reggio Calabria,
Catanzaro, Italy.
Funct Neurol 1995 May-Jun;10(3):151-5

ABSTRACT

The effect of systemic administration of pramiracetam on neuronal type nitric oxide synthase (NOS) activity and NOS mRNA expression were studied in the hippocampus and cerebral cortex in rats. A dose of 300 mg/kg (i.p.) of this nootropic produced an approximately 20% increase in NOS activity in rat brain cortical homogenates but not in hippocampal homogenates; no significant changes were observed in NOS mRNA expression in the cortex and hippocampus. A lower dose of pramiracetam (100 mg/kg i.p.) was ineffective on NOS mRNA expression and enzyme activity. Interestingly, administration of pramiracetam (300 mg/kg i.p.) in rats pretreated (24 h before) with lithium chloride (LiCl) (3 mEq/kg i.p.) yielded a 40% increase in cortical NOS activity. However, in LiCl-pretreated rats this nootropic failed to affect cortical NOS mRNA expression; LiCl (3 mEq/kg i.p.) given alone produced no effect. In conclusion, the present data demonstrate that pramiracetam given alone or in combination with LiCl increases NOS activity in brain cortical homogenates of rats and this may contribute to the mechanisms underlying learning and memory improvement produced by this nootropic.

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

And an article on NO and the brain:

http://www.sfn.org/i...eAndBrainDamage

Nitric Oxide and Brain Damage.
While researchers actively investigated larger molecules, the diminutive gas, nitric oxide, remained a wallflower. It was thought that the gas had no role in the body or brain. Today, nitric oxide is at center stage. It turns out that the molecule plays a role in a number of beneficial brain and body mechanisms. Recently researchers found evidence that it also can cause damage in the brain. The new understanding of its destructive side may lead to a whole new generation of medical treatments that can battle a variety of brain ailments.

A contributor to smog, nitric oxide (NO) once was known solely for its ability to pollute the environment. It forms in the air when nitrogen burns, for example during the production of car exhaust. Today researchers believe that the gas also can affect the brain.
Starting in the late 1980s, a large number of studies found that NO surprisingly exists in the body and brain and pervasively influences a number of biological functions. While many of its actions are beneficial, sometimes the molecule appears to turn toxic. Scientists are finding evidence that NO participates in the brain cell damage that occurs in a variety of neurological ailments, such as stroke and Parkinson's disease. The new research is leading to:

  • Targeted brain cell-protecting therapies that interfere with NO chemistry.
  • Clearer insight into the complex behavior of NO.
  • A better understanding of how gas compounds can impact biology.
For years, researchers were convinced that the tiny molecule consisting of a mere two atoms had no business in the body and brain. More complex compounds run many physiological processes so it made no sense that a gas could have an effect. Then in 1977 researchers determined that some of the drugs that are used to treat heart attacks by widening blood vessels, happen to release NO. Could NO naturally act to widen blood vessels in the body? Following a series of experiments, researchers concluded in 1986 that NO, indeed, regulates the widening of blood vessels. Research on NO snowballed. It turns out that NO influences a wide range of physiological functions. Among them, it appears to help the mechanisms that lead to memory and penile erection. Yes, NO mechanisms are behind the success of the well known impotence drug, Viagra.
Unfortunately you can get too much of a good thing.
Some researchers believe that many brain disorders can trigger an overproduction of NO. And the excess gas ends the life of brain cells known as neurons.
The first inkling of NO's sinister side came in 1991 when researchers found that they could block the neuron death that normally occurs in a cell model of stroke by inhibiting NO production. Specifically, they blocked the activity of an enzyme, known as nitric oxide synthase (NOS). This enzyme synthesizes the NO gas. Researchers have difficulty blocking NO directly because the gas has a very short lifespan in the neuron.
Additional research on animals also shows that NO is involved in neuron death. For example, studies determined that blocking NOS in the brain impedes the cell death that occurs from stroke as well as in other disorders such as Parkinson's disease.
Researchers now are actively investigating compounds that can derail NOS, in order to create new therapies that will control NO and protect human neurons in a range of brain ailments.
Scientists also are investigating other participants in NO's course of action in order to identify additional treatment targets. One participant that may hold promise is the enzyme called PARP. Some researchers believe that excess NO creates nicks and breaks in the DNA of neurons. The injuries in this important molecule activate PARP, which depletes energy sources in the cell, causing cell death. Scientists found that doses of small molecules that inhibit PARP reduce brain damage in a variety of animal stroke models. In addition, genetically-altered mice that do not produce PARP are protected from the damage of experimentally-induced stroke and Parkinson's disease.

Posted Image
Researchers believe that nitric oxide (NO) forms in neurons following a series of molecular reactions that occur in a matter of milliseconds. Many of the specifics of NO production are still unclear. For example, it's not known how often NO is produced or how involved different participants need to be in order to carry out the production. It's thought that the molecule glutamate can start the process by leaving a neuron and attaching to a molecule lining an adjacent neuron, known as the NMDA receptor. Their union causes calcium molecules to enter the receiving cell. This can trigger the activation of the enzyme NOS, which synthesizes NO. Some researchers believe that NO production normally aids brain function, but overproduction of the gas can kill neurons. A larger, higher resolution version of the graphic is <a href="http://www.sfn.org/s...llus.large.jpg" target="_blank">available here[/url]. (57k)

Illustration by Lydia Kibiuk, Copyright © 1999 Lydia Kibiuk.

Edited by chrono, 25 August 2010 - 04:28 PM.
formatting


#32 jackinbox

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Posted 24 December 2007 - 04:59 AM

I always tried Aniracetam at 750 - 1500 mg dosage without much success.. Some says it might be too much and recommend dosage around 250 mg. What you think of that?

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#33 meursault

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Posted 25 December 2007 - 10:01 PM

I always tried Aniracetam at 750 - 1500 mg dosage without much success.. Some says it might be too much and recommend dosage around 250 mg. What you think of that?


I like using that kind of dose, usually I take below 700mg. I find that instead of being lost in thoughts, I am able to focus my imagination.

#34 DAMABO

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Posted 11 February 2011 - 07:29 PM

Why do you want to avoid NO (assuming you mean Nitric Oxide)?


Current research shows that NO might have benfical or detrimental effects on the brain.
I don't want to mess with it, therefore.

Here is the article on Pramiracetam and NO.

http://www.biopsychi...amiracetam.html

Systemic administration of pramiracetam increases
nitric oxide synthase activity in the cerebral cortex of the rat
by
Corasaniti MT, Paoletti AM, Palma E,
Granato T, Navarra M, Nistico G.
Faculty of Pharmacy,
University of Reggio Calabria,
Catanzaro, Italy.
Funct Neurol 1995 May-Jun;10(3):151-5

ABSTRACT

The effect of systemic administration of pramiracetam on neuronal type nitric oxide synthase (NOS) activity and NOS mRNA expression were studied in the hippocampus and cerebral cortex in rats. A dose of 300 mg/kg (i.p.) of this nootropic produced an approximately 20% increase in NOS activity in rat brain cortical homogenates but not in hippocampal homogenates; no significant changes were observed in NOS mRNA expression in the cortex and hippocampus. A lower dose of pramiracetam (100 mg/kg i.p.) was ineffective on NOS mRNA expression and enzyme activity. Interestingly, administration of pramiracetam (300 mg/kg i.p.) in rats pretreated (24 h before) with lithium chloride (LiCl) (3 mEq/kg i.p.) yielded a 40% increase in cortical NOS activity. However, in LiCl-pretreated rats this nootropic failed to affect cortical NOS mRNA expression; LiCl (3 mEq/kg i.p.) given alone produced no effect. In conclusion, the present data demonstrate that pramiracetam given alone or in combination with LiCl increases NOS activity in brain cortical homogenates of rats and this may contribute to the mechanisms underlying learning and memory improvement produced by this nootropic.

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

And an article on NO and the brain:

http://www.sfn.org/i...eAndBrainDamage

Nitric Oxide and Brain Damage.
While researchers actively investigated larger molecules, the diminutive gas, nitric oxide, remained a wallflower. It was thought that the gas had no role in the body or brain. Today, nitric oxide is at center stage. It turns out that the molecule plays a role in a number of beneficial brain and body mechanisms. Recently researchers found evidence that it also can cause damage in the brain. The new understanding of its destructive side may lead to a whole new generation of medical treatments that can battle a variety of brain ailments.

A contributor to smog, nitric oxide (NO) once was known solely for its ability to pollute the environment. It forms in the air when nitrogen burns, for example during the production of car exhaust. Today researchers believe that the gas also can affect the brain.
Starting in the late 1980s, a large number of studies found that NO surprisingly exists in the body and brain and pervasively influences a number of biological functions. While many of its actions are beneficial, sometimes the molecule appears to turn toxic. Scientists are finding evidence that NO participates in the brain cell damage that occurs in a variety of neurological ailments, such as stroke and Parkinson's disease. The new research is leading to:

  • Targeted brain cell-protecting therapies that interfere with NO chemistry.
  • Clearer insight into the complex behavior of NO.
  • A better understanding of how gas compounds can impact biology.
For years, researchers were convinced that the tiny molecule consisting of a mere two atoms had no business in the body and brain. More complex compounds run many physiological processes so it made no sense that a gas could have an effect. Then in 1977 researchers determined that some of the drugs that are used to treat heart attacks by widening blood vessels, happen to release NO. Could NO naturally act to widen blood vessels in the body? Following a series of experiments, researchers concluded in 1986 that NO, indeed, regulates the widening of blood vessels. Research on NO snowballed. It turns out that NO influences a wide range of physiological functions. Among them, it appears to help the mechanisms that lead to memory and penile erection. Yes, NO mechanisms are behind the success of the well known impotence drug, Viagra.
Unfortunately you can get too much of a good thing.
Some researchers believe that many brain disorders can trigger an overproduction of NO. And the excess gas ends the life of brain cells known as neurons.
The first inkling of NO's sinister side came in 1991 when researchers found that they could block the neuron death that normally occurs in a cell model of stroke by inhibiting NO production. Specifically, they blocked the activity of an enzyme, known as nitric oxide synthase (NOS). This enzyme synthesizes the NO gas. Researchers have difficulty blocking NO directly because the gas has a very short lifespan in the neuron.
Additional research on animals also shows that NO is involved in neuron death. For example, studies determined that blocking NOS in the brain impedes the cell death that occurs from stroke as well as in other disorders such as Parkinson's disease.
Researchers now are actively investigating compounds that can derail NOS, in order to create new therapies that will control NO and protect human neurons in a range of brain ailments.
Scientists also are investigating other participants in NO's course of action in order to identify additional treatment targets. One participant that may hold promise is the enzyme called PARP. Some researchers believe that excess NO creates nicks and breaks in the DNA of neurons. The injuries in this important molecule activate PARP, which depletes energy sources in the cell, causing cell death. Scientists found that doses of small molecules that inhibit PARP reduce brain damage in a variety of animal stroke models. In addition, genetically-altered mice that do not produce PARP are protected from the damage of experimentally-induced stroke and Parkinson's disease.

Posted Image
Researchers believe that nitric oxide (NO) forms in neurons following a series of molecular reactions that occur in a matter of milliseconds. Many of the specifics of NO production are still unclear. For example, it's not known how often NO is produced or how involved different participants need to be in order to carry out the production. It's thought that the molecule glutamate can start the process by leaving a neuron and attaching to a molecule lining an adjacent neuron, known as the NMDA receptor. Their union causes calcium molecules to enter the receiving cell. This can trigger the activation of the enzyme NOS, which synthesizes NO. Some researchers believe that NO production normally aids brain function, but overproduction of the gas can kill neurons. A larger, higher resolution version of the graphic is <a href="http://www.sfn.org/s...llus.large.jpg" target="_blank">available here[/url]. (57k)

Illustration by Lydia Kibiuk, Copyright © 1999 Lydia Kibiuk.




perhaps we must consider the dosage here: 300mg/kg equates to 24 grams (ever took more than this?)or so in humans, that is, if humans have comparable reactions

#35 DAMABO

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Posted 11 February 2011 - 07:38 PM

The monoamine oxidase-B (MAO-B) inhibitor L-deprenyl (Selegiline) is effective in treating Parkinson's disease and possibly Alzheimer's disease, with a concomitant extension of life span. It has been suggested that the therapeutic efficacy of L-deprenyl may involve actions other than the inhibition of the enzyme MAO-B. This article reviews some novel actions of L-deprenyl and suggests that stimulation of nitric oxide (NO) production could be central to the action of the drug. L-Deprenyl induced rapid increases in NO production in brain tissue and cerebral blood vessels. In vitro or in vivo application of L-deprenyl produced vasodilatation. The drug also protected the vascular endothelium from the toxic effects of amyloid-beta peptide. Because NO modulates activities including cerebral blood flow and memory, and reduced NO production has been observed in AD brain, stimulation of NO production by L-deprenyl could contribute to the enhancement of cognitive function in AD. MAO-B inhibitors are unique in that they exert protective effects on both vascular and neuronal tissue and thus warrant further consideration in the treatment of vascular and neurodegenerative diseases associated with aging.

and NO doesn't seem so bad

#36 longevitynow

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Posted 12 February 2011 - 12:45 AM

In general I have noticed much more of an effect from Piracetam. With ANi I typically don't notice much, although in a perhaps too high dose it completely turned me into an emotionless Spock when I gave a speech. I felt focused, but recorded it and indeed, my affect was completely and noticeably flat.

#37 Bardamu

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Posted 28 February 2011 - 11:51 PM

Since I began my piracetam regimen I noticed a marked increase in visual memory, capacity for empathy, short and long term recall (I can memorize phone numbers in a snap; Piracetam also unearthed many fond childhood memories I had not pondered for years), creativity/fluid intelligence, audial and visual perception, expressivity of body language and speech, etc.

HOWEVER, I have experienced some negative side affects from Piracetam. I suspect this was because I was taking an attack dose (5g) for well over a month. Such experiences include drowsiness, spacing out, out-of-body experiences (I shit you not. Not necessarily bad, but I like to save those experiences for special occasians), depressive episodes, inability to carry out tasks requiring rote logic (ie reading a textbook), and a general feeling of "dreaminess" to life. Sounds great, you say? Not when "dreaminess" becames an everyday experience, thus trivializing the sensation. Trust me, work and school are not meant to be experienced in a Theta brainwave state. At least not on a daily basis.

I take 1.6-2.4g per day now, and I no longer experience the afforementioned effects. However, I suspect some of my negative experiences were due to dietary problems (ie lack of choline and/or glucose on particular days).
***
Aniracetam has a very noticeable stimulating effect for me, including mild vasoconstriction. My rote writing and reading speed (but not necesarily comprehension--Piracetam is better for reading/writing poetic stuff) is boosted noticeably, but the previous posters are absolutely right in saying that Aniracetam blunts your emotions. And no, stacking with Piracetam does not alleviate this affect. I take Ani only for writing papers and reading for long periods of time.

#38 Geovicsha

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Posted 13 September 2011 - 03:34 PM

I've ordered some Pramiracetam and Aniracetam and still awaiting its arrival; Piracetam is illegal to import in Australia without a prescription. Does Pramiracetam also affect creativity/theta waves?

#39 visualmagic

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Posted 18 September 2011 - 10:49 PM

Piracetam illegal to import to Australia? I've never heard that and order it here all the time.

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#40 Geovicsha

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Posted 24 September 2011 - 07:52 AM

Please respond to my PM, visualmagic.

Most of the accounts I read about Aniracetam was that it was anxiolytic and perhaps akin to mild stimulant qualities. The 750mg caps I’ve been having, however, make me sleepy and my brain in a complete foggy state. If anything, the fogginess heightens anxiety.

Although, having said that, I can see how it is sedative and makes you not worry. It also makes you more conscious of every thought you’re doing. It seems I need to cut the cap to about 375mg to get the best affects out of it.

Weird.




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