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Left Brain: NMDA/Piracetam Right Brain: AMPA/Aniracetam

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#1 Plasticperson

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Posted 22 January 2013 - 02:51 AM


As most of you know piracetam and aniracetam create different effects with the same goal in mine: cognitive enhancement. Based off of anecdotal report the difference in the effects seem to coincide with activation/enhancement of each hemisphere of the brain. Aniracetam would activate/enhance the right brain while the piracetem (and many of the other racetams) would enhance/activate the left brain. Both racetams exhibit modulation of different neurons; aniracetam modulates AMPA and NMDA and on the contrary piracetam mainly modulats NMDA. After stumbling upon this article http://www.scienceda...81117192918.htm and reading this portion:


They investigated the electron microscopic structure of synapses in left and right hippocampus, and found synapses made by terminals from the right hippocampus are large, complex in shape, and rich in the GluR1 subunit of AMPA-type glutamate receptors. In contrast, synapses receiving input from the left hippocampus are small and rich in the NR2B subunit of NMDA receptors. That means, both synaptic structure and synaptic molecules differ between synapses with left and right inputs.


One could easily deduct that this could be considered evidence of Aniracetams right brain effects and Piracetams left brain effects. What do you guys think?

Edited by Plasticperson, 22 January 2013 - 02:51 AM.

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#2 sparkk51

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Posted 22 January 2013 - 05:49 AM

I up-voted that post Plasticperson purely because I am so thankful that you're also curious about nootropic modulation of the brain's left and right hemispheres. I had long suspected piracetam, or at least racetams, to be the most appropriate for improving my left-bain thinking. Hopefully this thread proves to be usefull in the future.

Again, thank you so much!
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#3 LBGSHI

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Posted 22 January 2013 - 03:43 PM

A good hypothesis. Keep digging, and let us know what you find of interest.

#4 dirdir207

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Posted 22 January 2013 - 08:05 PM

Interesting theory, however I would like to point out that piracetam is also an allosteric regulator of AMPA and although with low occupation it does bind to one site that aniracetam does not that is unique to piracetam. I'm not sure whether new ampakines have been developed that act on this site. What is interesting however, is that this site is not normally used for neurotransmission.

Edited by dirdir207, 22 January 2013 - 08:05 PM.


#5 Rior

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Posted 22 January 2013 - 09:09 PM

Interesting theory, however I would like to point out that piracetam is also an allosteric regulator of AMPA and although with low occupation it does bind to one site that aniracetam does not that is unique to piracetam. I'm not sure whether new ampakines have been developed that act on this site. What is interesting however, is that this site is not normally used for neurotransmission.



Which particular site is this you're referring to? As far as I knew, Piracetam specifically as an allosteric modulator of the AMPA receptor with low affinity for the NMDAr and that's all. Granted, I haven't done any research into newfound studies for upwards of a year. Please fill me in!

#6 dirdir207

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Posted 22 January 2013 - 10:10 PM

Interesting theory, however I would like to point out that piracetam is also an allosteric regulator of AMPA and although with low occupation it does bind to one site that aniracetam does not that is unique to piracetam. I'm not sure whether new ampakines have been developed that act on this site. What is interesting however, is that this site is not normally used for neurotransmission.



Which particular site is this you're referring to? As far as I knew, Piracetam specifically as an allosteric modulator of the AMPA receptor with low affinity for the NMDAr and that's all. Granted, I haven't done any research into newfound studies for upwards of a year. Please fill me in!



http://www.ncbi.nlm....pubmed/20163115

"Piracetam also increases the maximal density of [AMPA glutamate receptors] in synaptic membranes from rat cortex due to the recruitment of a subset of AMPA receptors which do not normally contribute to synaptic transmission.”- I see this quote a lot, it is attributed to this study http://www.ncbi.nlm..../pubmed/8061686 however I don't see any mention of this in the abstract. Perhaps if someone could access the full text we could more easily verify this information.


edit: posted the wrong study initially.

I'm not sure why the top link sends you to the wrong study, so here is the main point:

" Both drugs bind to GluA2 and GluA3 in a very similar manner, suggesting little subunit specificity. However, the binding sites for piracetam and aniracetam differ considerably. Aniracetam binds to a symmetrical site at the center of the dimer interface. Piracetam binds to multiple sites along the dimer interface with low occupation, one of which is a unique binding site for potential allosteric modulators. This new site may be of importance in the design of new allosteric regulators."

Edited by dirdir207, 22 January 2013 - 10:08 PM.

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#7 Rior

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Posted 22 January 2013 - 10:24 PM

Nice. I don't know much about the dimer system, but I can work out the general gist pretty well. That's good to see. Has anyone had decent luck combining Aniracetam with Piracetam? That would obviously be my next question.

#8 machete234

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Posted 22 January 2013 - 10:57 PM

I combine 400mg of ani and 400mg of pira and that makes me less lazy than ani alone and I also dont find it as dysphoric as pira alone.
There is also not this drop that I get with ani after ~3hours its more gradual

#9 dirdir207

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Posted 22 January 2013 - 11:02 PM

For the life of me I cannot find the study right now, but I read earlier that chronic administration of piracetam and activation of AMPA leads to a DECREASE in piracetam efficacy.

#10 dirdir207

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Posted 22 January 2013 - 11:13 PM

http://www.ncbi.nlm....pubmed/21414388

"These results demonstrate similarities in EEG effects and their mediatory mechanisms for Piracetam and its much more effective analogue, Noopept. Activation of NMDA receptors is involved in the effects of a single injection of the nootropics, whereas activation of quisqualate/AMPA receptors is associated with the decrease in their efficacy after repeated use."
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#11 chung_pao

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Posted 22 January 2013 - 11:36 PM

http://www.ncbi.nlm....pubmed/21414388

"These results demonstrate similarities in EEG effects and their mediatory mechanisms for Piracetam and its much more effective analogue, Noopept. Activation of NMDA receptors is involved in the effects of a single injection of the nootropics, whereas activation of quisqualate/AMPA receptors is associated with the decrease in their efficacy after repeated use."


This definitely rings true. There's no comparison between my current effects of noopept/piracetam to that of my first doses.
I also find the desensitization to piracetam to have increased while only taking noopept, which indicates a similar mechanism of action.
I should probably decrease the frequency to increase its potency, like many others.
Although, if piracetam and aniracetam affects different areas, cycling could be useful to improve sensitivity.

Edited by chung_pao, 22 January 2013 - 11:38 PM.






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