17 replies to this topic

[Reformed-Redan]

I have been taking Oxiracetam on and off lately. I'm not sure about its effects; but, there is something working in the backgroud. I feel even younger again in cognitive functioning. Like I can pick up on thoguhts more easily. Like my brain is more receptive. But, I had an argument yesterday after taking oxiracetam. I woke up with this swishy swashy feeling. Like a litle bit after a hangover.

After reading about the most probable mechanism of action I am lead to believe that Piracetam "sensitizes" the brain (NMDA receptors) through permeability and "modulation of ion channels (i.e., Na⁺, K⁺))". Thus, I figured that neurotoxicity (excitotoxicity) in already young and more receptive brains might be of concern.

Excitotoxicity can occur from substances produced within the body (endogenous excitotoxins). Glutamate is a prime example of an excitotoxin in the brain, and it is also the major excitatory neurotransmitter in the mammalian CNS.^[9] During normal conditions, glutamate concentration can be increased up to 1mM in the synaptic cleft, which is rapidly decreased in the lapse of milliseconds.^[10] When the glutamate concentration around the synaptic cleft cannot be decreased or reaches higher levels, the neuron kills itself by a process called apoptosis.^{[11] [12]}

JUst someething worth mentioning.

Edited by redan, 15 January 2012 - 07:25 PM.

[absent minded]

After reading about the most probable mechanism of action I am lead to believe that Piracetam "sensitizes" the brain (NMDA receptors) through permeability and "modulation of ion channels (i.e., Na⁺, K⁺))".

Can this mean that it's easier to get soppy during emotional parts in movies ?

[Reformed-Redan]

After reading about the most probable mechanism of action I am lead to believe that Piracetam "sensitizes" the brain (NMDA receptors) through permeability and "modulation of ion channels (i.e., Na⁺, K⁺))".

Can this mean that it's easier to get soppy during emotional parts in movies ?

IDK, if it makes you feel that way. I'm just saying that Piracetam might lower the needed amount of glutamate for excitotoxicity to occur. Which doesn't sound like a good thing.

I've read on some other threads that Piracetam potentiates the effects of many drugs. The same should apply to excitotoxicity.

[Michael Campbell]

After reading about the most probable mechanism of action I am lead to believe that Piracetam "sensitizes" the brain (NMDA receptors) through permeability and "modulation of ion channels (i.e., Na⁺, K⁺))".

Can this mean that it's easier to get soppy during emotional parts in movies ?

God I hope not; I wear my emotions on my sleeve as it is!

[SuperjackDid_]

Magnesium and Alpha lipoic acid ,prevent me from Depression from Piracetam use.

Might involve in
excitotoxicity?


worth worth mentioning.

[absent minded]

and what about Huperzine A as insurance? But this one is apparantly dangerous for long-term usage.

[SuperjackDid_]

Huperzine A not suit for daily use,and NMDA antagonist might weak ,and ton of side effect

​i try experiment with it many time ,i get more deep depress .

[Reformed-Redan]

I got Taurine as a buffer, just in case. Wasn't looking forward to taking Lithium for excitotoxicity.

[SuperjackDid_]

Problem is Piracetam increase receptor density overtime and it cause over stimulation and cause cell death when continue use.

More good idea to try find maintain dose or stop it for a while until receptor get down regulation .
But Racetam not just only up receptor ,it do a lot of thing that i very keen to use it daily like mood boost ,blood flow ,creativity ,and other thing that other can't do.


Taurine um,i have some experience on it ,

Someday i take Piracetam and get very sleepy effect ,get my mood really depress ,unable to think or talk anything

i try take Taurine that time ,and i feel so much difference like i take Piracetam on first day,

but i try to repeat that step again ,but it fail to work consistently .

[Philosopher]

Piracetam does not cause excitotoxicity. If anyone thinks so, they are either inexperienced with piracetam or anxious.

[hooter]

Piracetam causes dopaminergic and serotonergic excitotoxicity if combined with amphetamine/cocaine/mdma. But on it's own, it's completely safe. It protects the brain.

[muhali3]

Piracetam does not cause excitotoxicity. It potentiates glutamatergic transmission but GABAergic transmission as well. The amount of glutamate needed to initiate excitotoxicity is very great. When such high levels are reached, there are very obvious and serious symptoms. If an excitotoxic event does happen in your brain, you will be very aware that something is seriously wrong. The biggest contraindication of piracetam is a reduced seizure threshold. As long as you don't have a seizure, you can be assured that there is no exictotoxicity resulting from piracetam use.

Edited by muhali3, 19 January 2012 - 04:16 AM.

[crobert]

Piracetam causes dopaminergic and serotonergic excitotoxicity if combined with amphetamine/cocaine/mdma. But on it's own, it's completely safe. It protects the brain.

Is there any potential for piracetam induced excitotoxicity when used concurrently with caffeine or MSG?

Edited by crobert, 10 May 2012 - 01:57 PM.

[medievil]

If anything id say it protects against it due to its antioxidant effects (oxidative stress plays a role in excitoxiticy).

[aaron43]

a by-product of my senior project...
and first post who knows how long..

This is in regards to preventing amphetamine-piracetam induced exitiotoxicity
Creatine is the answer to glutamate-induced exitotoxicity:

"In contrast, extracellular glutamate concentrations reflecting an overflow (and secondary hyperexcitability) which occurs along with oxidative stress were effectively reduced following creatine incubation (Fig. 5). Thus, creatine seems to efficiently interfere with this vicious circle which maintains the excitotoxic cascade after its initiation. Even under non-stressful baseline conditions glutamate concentrations remained reduced in creatine-treated hippocampal cell cultures."

"Following 18 h preincubation with 5 mM creatine (which yielded no significant toxicity) and careful washout, the rise of intracellular Ca2+ ions in response to NMDA receptor stimulation at supramaximal doses (1 mM) was almost completely abolished"

Edited by aaron43, 17 March 2013 - 02:46 AM.

[aaron43]

and this..

"Depletion of high-energy phosphates, such as ATP and phosphocreatine (PCr) is an early event in the neurotoxicity of
glutamate [24–27]. Abnormal calcium uptake into mitochondria has also been reported following exposure to glutamate [28–29]. Profound disruption of the cellular energy ultimately leads to a decreased GTP concentration [30] along with altered activity of GTP binding proteins, such as Rac and Ras, which yields a proapoptotic state [31]. Juravleva et al. [32] hypothesized that the maintainance of the cellular energy charge by creatine may shift the apoptotic balance towards the Ras-mediated antiapoptotic PI3K/AKT or survival signal pathways (PI3K/Rac/NAD(P)H- oxidase/ROS/NF-kappaB), specifically the Ras/NFkappaB sys- tem, where multiple pathways mediating survival converge via stabilization of GTP levels. Indeed, creatine was shown to maintain neuronal/glial survival following glutamate treatment, which correlated with decreased levels of farnesylated Ras and the NF-kappaB inhibitor IkappaB and increased levels of ROI [32]."

unrelated:
After being demeaned by the moderators of this website in the past as they said I did not have the accredation/knowledge to understand the information relative to this site, and being told I was the product of unintelligent bravery, that chance produced something worth nootropic value. Do not rest, stay consistent, learn, the only opinons that ever matter are your own, facts and logic reign. Do not underestimate the ability of goal-orientated-choice and the the significant changes it can induce on fundamental biochemical cascades. Choose enlightment every second, and you will see doors with exponential enlightenment values open up every minute. Do not be a victim to yourself. Do not identify yourself as dependent on an external molecule, I have a strong theory that self-identification of reliancy on anything external, pre-sets your biochemical levels towards producing a phenotypic response of submission and depression. The drugs won't get you, the concepts will.

Edited by aaron43, 17 March 2013 - 02:44 AM.

[aaron43]

In regards to creatine supplementation pharmocodynamics and it's relation to glutamate:

"Similarly, the glial high affinity glutamate transporter Slc1a3 was up-regulated in Cr-fed mice by a factor of 1.92."

[aaron43]

aw boo did i ruin the topic