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  1. #1
    Registered User Murderfox's Avatar
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    A new day has dawned... PROMETHEUS RISING Unveiled -WRITE UP-

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    Just in time for the new year!
    MAN Sports presents Prometheus Rising, the most innovative, muscle- and performance-enhancing formula MANkind has ever seen!

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    Prometheus Rising amplifies the internal anabolic environment for maximum gains in muscle size, strength and power. Prometheus Rising also contains ingredients included to prioritize fat utilization while supporting muscle growth and retention, for dramatic muscle “hardening” effect.
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    Prometheus Rising amplifies the body’s internal anabolic mechanisms, supports maximum volume and enhances muscular growth, featuring:

    D-Aspartic Acid (DAA), 3000mg: T-boosting: Recent studies have shown this non-essential amino acid to enhance LH and testosterone release, boosting testosterone levels up to 42%, and amplifying natural pituitary testicular stimulation. DAA is a safe and effective, natural alternative to illegal muscle-enhancing agents. *

    Coleus Forskohlii (10% forskolin) 500mg: Muscle-hardening: ramp up cAMP through modulation of the enzyme, adenylate cyclase. There are studies that suggest Coleus Forskohlii optimizes hormone levels to maximize muscle-building, while supporting fat utilization, for a leaner, harder and more muscular look. *

    Agmatine, 1000mg: (GH/IGF-1 up-regulation, all day pump, powerful anti-oxidant properties) Agmatine may well be the true “Holy Grail” of sports nutrition. It’s a metabolite of Arginine, and has many different functions that are valuable to athletes. Agmatine goes way beyond Arginine, including ramped up GH and IGF-1 output, increased LH output, increased insulin sensitivity and increased NO production. In addition to bolstering the endocrine system to maximize anabolism, Agmatine enhances blood flow to muscle tissues, for greater nutrient and oxygen infusion for improved performance, increased muscle size and fullness and quicker recovery. *

    R-Alpha-Lipoic Acid, 300mg: R-ALA is a potent anti-oxidant that neutralizes potentially harmful cellular pollutants, supporting cellular integrity and optimizing cell health and function. R-ALA also serves as a glucose disposal agent and cellular energy catalyst, working within the muscle cells to increase nutrient absorption, attenuate insulin-spike and enhance physical performance. *

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    *These statements have not been evaluated by the FDA. This product is not intended to diagnose, treat, cure or prevent any disease.

    References:
    D’Aniello A, Di Cosmo A, et al. Involvement of D-aspartic acid in the synthesis of testosterone in rat testes. Life Sci, 1996;59(2):97-104.
    D’Aniello A. D-Aspartic acid: an endogenous amino acid with an important neuroendocrine role. Brain Res Rev, 2007 Feb;53(2):215-34.

    D’Aniello, A. D-Aspartic Acid regulates the release and synthesis of LH and testosterone in human. The Lancet,
    Godard, M, Johnson, B and Richmond, S. Body Compositon and Hormonal Adaptations Associated with Forskolin Consumption in Overweight and Obese Men. Obesity Research, (2005) 13, 1335–1343.
    Jae-Hwan Kim, et al. Agmatine reduces infarct area in a mouse model of transient focal cerebral ischemia and protects cultured neurons from ischemia-like injury. Experimental Neurology. 189 (2004) 122– 130.
    Satriano, J, et al. An emerging role for agmatine. Kidney Int. 56, (1999) 1252-53
    Topo E, Soricelli A, et al. The role and molecular mechanism of D-aspartic acid in the release and synthesis of LH and testosterone in humans and rats. Reprod Biol Endocrinol, 2009 Oct 27;7:120.

    IN WALKS PROMETHEUS, RISING™!

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  2. #2
    Registered User zeebodybuilder's Avatar
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    1st
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  3. #3
    Registered BroScientist quank's Avatar
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    2nd
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  4. #4
    Registered User JornT's Avatar
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    DAA is an NMDA angonist and Agmatine a NMDA antagonist I believe, curious to see some discussion on how they would interact together.
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  5. #5
    Registered User Murderfox's Avatar
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    Originally Posted by JornT View Post
    DAA is an NMDA angonist and Agmatine a NMDA antagonist I believe, curious to see some discussion on how they would interact together.
    While that it is true for both, i have not seen any studies or further in depth discussions where a problem may arise from the simultaneous use of DAA and Agmatine.
    Last edited by Murderfox; 12-31-2010 at 09:57 AM.
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  6. #6
    Misc Section OG Freedirt's Avatar
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    Very nice
    Misc section, OG of The Gangsta Nation.

    ₪ ₪ ₪TRUE MI$CER₪ ₪ ₪

    German/African/Native American Genetics. You jelly?

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  7. #7
    Registered User Oscarizo's Avatar
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    Thanks for the notice on these product man.
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  8. #8
    Registered User llllern's Avatar
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    Let's see what you gurus have to say about our latest creation

    I for one am very excited about this product
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  9. #9
    Registered User carbcrazy's Avatar
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    looks pretty dope haha, word?!
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  10. #10
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    looks goood can i have some :P
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  11. #11
    Registered User SShred32's Avatar
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    Still love.the.name. So much. And the profile looks very nice and developed so I am interested to see how people like this product! Go MAN
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  12. #12
    Teach Me How to Dougie asianstyles's Avatar
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    looks awesome MAN
    Not affiliated
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  13. #13
    Registered User GBROS's Avatar
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    OMG i think i just wee'd myself with that packaging alone.
    Proprietary blended companies' worst nightmare.


    Oh well. Money doesn't grow on trees [although apparently, it does grow on pond weeds]. - NO HYPE
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  14. #14
    Registered User GBROS's Avatar
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    Originally Posted by JornT View Post
    DAA is an NMDA angonist and Agmatine a NMDA antagonist I believe, curious to see some discussion on how they would interact together.
    Time for Dr P
    Proprietary blended companies' worst nightmare.


    Oh well. Money doesn't grow on trees [although apparently, it does grow on pond weeds]. - NO HYPE
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  15. #15
    Registered User llllern's Avatar
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    Callig all dr's to the thread
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  16. #16
    Registered User GBROS's Avatar
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    Originally Posted by llllern View Post
    Callig all dr's to the thread
    You make it sound like a call to superheroes. I guess someone's been spending their holidays all glued up watching action hero films.
    Proprietary blended companies' worst nightmare.


    Oh well. Money doesn't grow on trees [although apparently, it does grow on pond weeds]. - NO HYPE
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  17. #17
    Registered User llllern's Avatar
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    Originally Posted by GBROS View Post
    You make it sound like a call to superheroes. I guess someone's been spending their holidays all glued up watching action hero films.
    Well I have been sick for 3 weeks lol
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  18. #18
    Platinum Member eldawg's Avatar
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    Originally Posted by llllern View Post
    Let's see what you gurus have to say about our latest creation

    I for one am very excited about this product
    Originally Posted by llllern View Post
    Callig all dr's to the thread
    I may be mistaken, but it sounds like you are asking members to vet this product?


    (I don't think you are going to get much of a discussion in the Company Promo section)
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  19. #19
    Registered User GBROS's Avatar
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    Originally Posted by llllern View Post
    Well I have been sick for 3 weeks lol
    Along with the rest of the people becoming sick around this time lol.
    Proprietary blended companies' worst nightmare.


    Oh well. Money doesn't grow on trees [although apparently, it does grow on pond weeds]. - NO HYPE
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  20. #20
    Humble Bro On Fire's Avatar
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    Originally Posted by eldawg View Post
    (I don't think you are going to get much of a discussion in the Company Promo section)
    Indeed. This is the section where dudes hang off your nuts in attempt to score free product.

    Neat looking formula btw, another potential natty-t-booster. Could be a handy addition to a prescription pct.
    Don't tell me what you want to do, do it.
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    Working on my "core", because I'm not a fat fuk.
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  21. #21
    Primum non nocere Synapsin's Avatar
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    Originally Posted by eldawg View Post
    I may be mistaken, but it sounds like you are asking members to vet this product?


    (I don't think you are going to get much of a discussion in the Company Promo section)
    I wrote about something similar to this else where, so let me go into some detail about the NMDA receptor (easy to find anywhere, nothing original here besides some concepts I was personally toying with, and I should note it was done on my phone so don't get mad if my grammar is poor):


    "The NMDA receptor is an ionotropic receptor that allows for the transfer of electrical signals between neurons in the brain and in the spinal column. For electrical signals to pass, the NMDA receptor must be open. To remain open, an NMDA receptor must bind to glutamate and to glycine. An NMDA receptor that is bound to glycine and glutamate and has an open ion channel is called "activated."

    NMDA receptors aren't activated easily. The receptor is blocked by Mg2+ so it needs to have sufficient depolarization. Even if you have Aspartic acid there (or Glutamate), you need Glycine to be there as well. So you need a few things at once to activate the NMDA receptors, the key thing being the depolarization of say an AMPA receptor near by before any of the binding even matters. Test force gets around the issue of Glycine by using Sarcosine.

    NMDA receptors have different subunits, and the effects of the subunits upon activation. Basic message to take home is that DAA is likely not going to elicit toxicity (due to A and B noted below) because toxicity most likely only comes from NR2B subunit. But if it DOES elicist neurotoxicity, keep reading on how to address this.


    A) NR2B-NR2A developmental switch (hypothesis)
    B) NR2A probably has a higher affinity than NR2B when it comes L/D-Aspartate


    Chemicals that deactivate the NMDA receptor are called antagonists. NMDAR antagonists fall into four categories:

    1) Competitive antagonists, which bind to and block the binding site of the neurotransmitter glutamate;
    2) Glycine antagonists, which bind to and block the glycine site;
    3) Noncompetitive antagonists, which inhibit NMDARs by binding to allosteric sites; and
    4) Uncompetitive antagonists, which block the ion channel by binding to a site within it."

    Something worthy of a read:

    "Agmatine Selectively Blocks theN-Methyl-d-Aspartate Subclass of Glutamate Receptor Channels in Rat Hippocampal Neurons1

    Abstract

    We investigated in rat hippocampus neurons whether 4-(aminobutyl)guanidine (agmatine), formed by decarboxylation ofl-arginine by arginine decarboxylase and metabolized to urea and putrescine, can modulate the function ofN-methyl-d-aspartate (NMDA) receptor channels. In cultured hippocampal neurons studied by whole-cell patch clamp, extracellular-applied agmatine produced a voltage- and concentration-dependent block of NMDA but not α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid nor kainate currents. Analysis of the voltage dependence of the block suggests that agmatine binds at a site located within the NMDA channel pore with a dissociation constant of 952 μM at 0 mV and an electric distance of 0.62. We also tested effects of several agmatine analogs. Arcaine (1,4-butyldiguanidine) also produced a similar voltage-dependent block of the NMDA current, whereas putrescine (1,4-butyldiamine) had little effect, suggesting that the guanidine group of agmatine is the active moiety when blocking the NMDA channel. Moreover, spermine (an endogenous polyamine) potentiated the NMDA current even in the presence of blocker agmatine or arcaine, suggesting that the guanidine-containing compounds agmatine and arcaine interact with the NMDA channel at a binding site different from that of spermine. Our results indicate that in hippocampal neurons agmatine selectively modulates the NMDA subclass of glutamate receptor channels mediated by the interaction between the guanidine group and the channel pore. The results support other data that agmatine may function as an endogenous neurotransmitter/neuromodulator in brain."

    Also:

    Effect of Agmatine Against Cell Death Induced by NMDA and Glutamate in Neurons and PC12 Cells

    "Therefore, it is conceivable that agmatine, coreleased with glutamate, may act to
    inhibit the activation of NMDA receptors during conditions leading to higher glutamate
    release. Further in vivo studies, measuring the release of agmatine along with
    glutamate are required to verify this hypothesis.
    In summary, we have provided evidence that agmatine is a neuroprotective
    molecule and reduces excitotoxic cell death induced by glutamate or NMDA.

    .....

    Agmatine protects against cell damage induced by NMDA and glutamate in cultured hippocampal neurons."

    "Taken together, these results demonstrate that agmatine can protect cultured hippocampal neurons from NMDA- or glutamate-induced excitotoxicity, through a possible blockade of the NMDA receptor channels or a potential anti-apoptotic property."

    Another thing to keep in mind from the paper I just pasted above:

    "Because axons that innervate pyramidal cells are glutamatergic and
    pyramidal cells expressNMDAsubclass of glutamate receptors, it has been proposed
    that agmatine may be costored and released with glutamate as a counterregulatory
    molecule. Electrophysiological studies of cultured hippocampal neurons have also
    supported the contention that agmatine selectively inhibitedNMDAchannels (Yang
    and Reis, 1999).

    While these previous studies suggested a possible regulatory role for agmatine
    in normal glutamatergic neurotransmission, agmatine may also play a role in pathological conditions involving higher activation ofNMDAreceptors. Thus, agmatine
    is protective against ischemic injury (Gilad, 1996b), spinal cord injury (Fairbanks
    et al., 2000; Gilad and Gilad 2000; Yu et al., 2000) and neuropathic pain (Fairbanks
    et al., 1998), conditions that arise from higher NMDA receptor activation and are
    reversed byNMDAreceptor antagonists. The present study has provided further evidence
    that the neuroprotective action of agmatine could be mediated by the blockade
    of NMDA receptors."

    Dr. Houser was actually asked this before (http://www.leanbulk.com/forum/ask-dr...-question.html)

    Anyhow, I wrote a post about this on a different forum concerning DAA and something with a similar concept to Agmatine in terms of neuroprotective methods, Huperzine A.

    Some key differences though:

    "Agmatine Fails to Inhibit Cell Death Induced by Calcimycin or Staurosporin
    To address the question whether the effect of agmatine on cell death is mediated
    by nonspecific blockade of cation channels or by inhibiting intracellular protein
    kinase pathways, we investigated other nonexcitoxic cell death models. Calcimycin,
    a calcium channel opener, caused a significant increase in LDH release in neurons
    (4% vs. 11.5%) and PC12 (4% vs. 12%) cells, indicating marked cell death (Fig. 5).
    Agmatine (100 ¹M), when incubated with calcimycin, failed to inhibit the elevated
    release of LDH.Asimilar result was obtained with staurosporin, which causes apoptotic
    cell death by intracellular actions, where LDH release was not inhibited by
    agmatine (100 ¹M) in neurons and PC12 cells (Fig. 5)."

    What I said about Huperzine A:


    "Huperzine A (?100 µM) had no effect on the binding of [3H]glutamate (low- and high-affinity glutamate sites), [3H]MDL 105,519 (NMDA glycine regulatory site), [3H]ifenprodil (NMDA polyamine site) or [3H]CGS 19755 (NMDA antagonist). These are the things we really worry about when we talk about DAA and NMDA receptors.

    In contrast with these results, HUP-A non-competitively (Hill slope < 1) inhibited [3H]MK-801 and [3H]TCP binding (co-located NMDA ion channel PCP site) with pseudo Ki ? 6 µM.

    Therefore, HUP-A most likely attenuates excitatory amino acid toxicity by blocking the NMDA ion channel and subsequent Ca2+ mobilization at or near the PCP and MK-801 ligand sites."

    Now that we have all that said, key thing to keep in mind, once the NMDA receptor is activated (takes a few things to be activated), that is it, it will release the neurotransmitter. If glutamate induced NMDA activation is co-activated with Agmatine release, I would assume that taking DAA will also increase endogenous Agmatine release in order to protect you from glutamatergic neurotoxicity. We can sort of thing of Agmatine as acting as a buffer to keep DAA from over exciting NDMA receptors.
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  22. #22
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    Originally Posted by Synapsin View Post
    I wrote about something similar to this else where, so let me go into some detail about the NMDA receptor (easy to find anywhere, nothing original here besides some concepts I was personally toying with, and I should note it was done on my phone so don't get mad if my grammar is poor):


    "The NMDA receptor is an ionotropic receptor that allows for the transfer of electrical signals between neurons in the brain and in the spinal column. For electrical signals to pass, the NMDA receptor must be open. To remain open, an NMDA receptor must bind to glutamate and to glycine. An NMDA receptor that is bound to glycine and glutamate and has an open ion channel is called "activated."

    NMDA receptors aren't activated easily. The receptor is blocked by Mg2+ so it needs to have sufficient depolarization. Even if you have Aspartic acid there (or Glutamate), you need Glycine to be there as well. So you need a few things at once to activate the NMDA receptors, the key thing being the depolarization of say an AMPA receptor near by before any of the binding even matters. Test force gets around the issue of Glycine by using Sarcosine.

    NMDA receptors have different subunits, and the effects of the subunits upon activation. Basic message to take home is that DAA is likely not going to elicit toxicity (due to A and B noted below) because toxicity most likely only comes from NR2B subunit. But if it DOES elicist neurotoxicity, keep reading on how to address this.


    A) NR2B-NR2A developmental switch (hypothesis)
    B) NR2A probably has a higher affinity than NR2B when it comes L/D-Aspartate


    Chemicals that deactivate the NMDA receptor are called antagonists. NMDAR antagonists fall into four categories:

    1) Competitive antagonists, which bind to and block the binding site of the neurotransmitter glutamate;
    2) Glycine antagonists, which bind to and block the glycine site;
    3) Noncompetitive antagonists, which inhibit NMDARs by binding to allosteric sites; and
    4) Uncompetitive antagonists, which block the ion channel by binding to a site within it."

    Something worthy of a read:

    "Agmatine Selectively Blocks theN-Methyl-d-Aspartate Subclass of Glutamate Receptor Channels in Rat Hippocampal Neurons1

    Abstract

    We investigated in rat hippocampus neurons whether 4-(aminobutyl)guanidine (agmatine), formed by decarboxylation ofl-arginine by arginine decarboxylase and metabolized to urea and putrescine, can modulate the function ofN-methyl-d-aspartate (NMDA) receptor channels. In cultured hippocampal neurons studied by whole-cell patch clamp, extracellular-applied agmatine produced a voltage- and concentration-dependent block of NMDA but not α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid nor kainate currents. Analysis of the voltage dependence of the block suggests that agmatine binds at a site located within the NMDA channel pore with a dissociation constant of 952 μM at 0 mV and an electric distance of 0.62. We also tested effects of several agmatine analogs. Arcaine (1,4-butyldiguanidine) also produced a similar voltage-dependent block of the NMDA current, whereas putrescine (1,4-butyldiamine) had little effect, suggesting that the guanidine group of agmatine is the active moiety when blocking the NMDA channel. Moreover, spermine (an endogenous polyamine) potentiated the NMDA current even in the presence of blocker agmatine or arcaine, suggesting that the guanidine-containing compounds agmatine and arcaine interact with the NMDA channel at a binding site different from that of spermine. Our results indicate that in hippocampal neurons agmatine selectively modulates the NMDA subclass of glutamate receptor channels mediated by the interaction between the guanidine group and the channel pore. The results support other data that agmatine may function as an endogenous neurotransmitter/neuromodulator in brain."

    Also:

    Effect of Agmatine Against Cell Death Induced by NMDA and Glutamate in Neurons and PC12 Cells

    "Therefore, it is conceivable that agmatine, coreleased with glutamate, may act to
    inhibit the activation of NMDA receptors during conditions leading to higher glutamate
    release. Further in vivo studies, measuring the release of agmatine along with
    glutamate are required to verify this hypothesis.
    In summary, we have provided evidence that agmatine is a neuroprotective
    molecule and reduces excitotoxic cell death induced by glutamate or NMDA.

    .....

    Agmatine protects against cell damage induced by NMDA and glutamate in cultured hippocampal neurons."

    "Taken together, these results demonstrate that agmatine can protect cultured hippocampal neurons from NMDA- or glutamate-induced excitotoxicity, through a possible blockade of the NMDA receptor channels or a potential anti-apoptotic property."

    Another thing to keep in mind from the paper I just pasted above:

    "Because axons that innervate pyramidal cells are glutamatergic and
    pyramidal cells expressNMDAsubclass of glutamate receptors, it has been proposed
    that agmatine may be costored and released with glutamate as a counterregulatory
    molecule. Electrophysiological studies of cultured hippocampal neurons have also
    supported the contention that agmatine selectively inhibitedNMDAchannels (Yang
    and Reis, 1999).

    While these previous studies suggested a possible regulatory role for agmatine
    in normal glutamatergic neurotransmission, agmatine may also play a role in pathological conditions involving higher activation ofNMDAreceptors. Thus, agmatine
    is protective against ischemic injury (Gilad, 1996b), spinal cord injury (Fairbanks
    et al., 2000; Gilad and Gilad 2000; Yu et al., 2000) and neuropathic pain (Fairbanks
    et al., 1998), conditions that arise from higher NMDA receptor activation and are
    reversed byNMDAreceptor antagonists. The present study has provided further evidence
    that the neuroprotective action of agmatine could be mediated by the blockade
    of NMDA receptors."

    Dr. Houser was actually asked this before (http://www.leanbulk.com/forum/ask-dr...-question.html)

    Anyhow, I wrote a post about this on a different forum concerning DAA and something with a similar concept to Agmatine in terms of neuroprotective methods, Huperzine A.

    Some key differences though:

    "Agmatine Fails to Inhibit Cell Death Induced by Calcimycin or Staurosporin
    To address the question whether the effect of agmatine on cell death is mediated
    by nonspecific blockade of cation channels or by inhibiting intracellular protein
    kinase pathways, we investigated other nonexcitoxic cell death models. Calcimycin,
    a calcium channel opener, caused a significant increase in LDH release in neurons
    (4% vs. 11.5%) and PC12 (4% vs. 12%) cells, indicating marked cell death (Fig. 5).
    Agmatine (100 ¹M), when incubated with calcimycin, failed to inhibit the elevated
    release of LDH.Asimilar result was obtained with staurosporin, which causes apoptotic
    cell death by intracellular actions, where LDH release was not inhibited by
    agmatine (100 ¹M) in neurons and PC12 cells (Fig. 5)."

    What I said about Huperzine A:


    "Huperzine A (?100 µM) had no effect on the binding of [3H]glutamate (low- and high-affinity glutamate sites), [3H]MDL 105,519 (NMDA glycine regulatory site), [3H]ifenprodil (NMDA polyamine site) or [3H]CGS 19755 (NMDA antagonist). These are the things we really worry about when we talk about DAA and NMDA receptors.

    In contrast with these results, HUP-A non-competitively (Hill slope < 1) inhibited [3H]MK-801 and [3H]TCP binding (co-located NMDA ion channel PCP site) with pseudo Ki ? 6 µM.

    Therefore, HUP-A most likely attenuates excitatory amino acid toxicity by blocking the NMDA ion channel and subsequent Ca2+ mobilization at or near the PCP and MK-801 ligand sites."

    Now that we have all that said, key thing to keep in mind, once the NMDA receptor is activated (takes a few things to be activated), that is it, it will release the neurotransmitter. If glutamate induced NMDA activation is co-activated with Agmatine release, I would assume that taking DAA will also increase endogenous Agmatine release in order to protect you from glutamatergic neurotoxicity. We can sort of thing of Agmatine as acting as a buffer to keep DAA from over exciting NDMA receptors.
    Translation for us non-brainchilds....
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  23. #23
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    Originally Posted by eldawg View Post
    I may be mistaken, but it sounds like you are asking members to vet this product?


    (I don't think you are going to get much of a discussion in the Company Promo section)
    no not really this is a write up but in the end I would like to hear what people think about the product .
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  24. #24
    Primum non nocere Synapsin's Avatar
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    Originally Posted by _J-BONE_ View Post
    Translation for us non-brainchilds....
    Well, this is what I think:

    We have DAA present (check, so more NMDA activation now with Glycine, Ca+2 current, agonist DAA here), Agmatine doesn't affect Calcium intracellular mechanisms (check, you need the depolarization to stop the Mg+2 from blocking the site), Glycine present (will happen for activation of the receptor, so check). Say the NMDA receptor is now activated, releases Glutamate, blah blah blah, the Agmatine in the product in theory based on what I posted above is also endogenously released, so exogenous application will enhance that regulatory role of Agmatine so that in higher levels of NMDA receptor activation, it will inhibit the receptor from higher glutamate release (so overexcitation leading to potential neurotoxicity) by inhibting the receptor. Basically Agmatine might be able to prevent the neurotoxicity you always hear about when talking about DAA by preventing overexcitation of NMDA receptors/ reversing the levels of activation.
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  25. #25
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    Originally Posted by Synapsin View Post
    Basically Agmatine might be able to prevent the neurotoxicity you always hear about when talking about DAA by preventing overexcitation of NMDA receptors/ reversing the levels of activation.
    Interesting. I like Synapsin's posts.
    Don't tell me what you want to do, do it.
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  26. #26
    Banned G.W. Hayduke's Avatar
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    Originally Posted by On Fire View Post
    Interesting. I like Synapsin's posts.
    me three!
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  27. #27
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    synapsin is a good dude

    if you ever have a stroke, then take agmatine after
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  28. #28
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    Originally Posted by michael3435 View Post
    if you ever have a stroke, then take agmatine after
    'cause chicks don't mind if half your body is limp so long as you're yoked.
    Originally Posted by On Fire View Post
    Indeed. This is the section where dudes hang off your nuts in attempt to score free product.
    Who told you my mission statement?
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  29. #29
    Primum non nocere Synapsin's Avatar
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    Originally Posted by On Fire View Post
    Interesting. I like Synapsin's posts.
    Originally Posted by G.W. Hayduke View Post
    me three!
    Originally Posted by michael3435 View Post
    synapsin is a good dude

    if you ever have a stroke, then take agmatine after
    Appreciate the kind words guys.
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    Whats the price point on this product?
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