Fasoracetam

[asecin]

Guys, aniractam has POWERFUL sertonergic and dopamiergic effects. this is most likely the cause for the depression.

http://www.sciencedirect.com/science/article/pii/S0006899301029390


http://onlinelibrary.wiley.com/doi/10.1111/j.1527-3458.2002.tb00216.x/pdf

No I haven't tried any selevtive racetams yet. I am very true into nootropics.

Originally Posted by Ligaturd
Aniracetams metabolite N-Anisoyl-GABA is a gaba receptor agonist (not sure about selectivity) but it modulates glutamate levels. It simultaneously has nootropic effects and anxiolytic effects. That combined with Coluracetam pretty much temporarily got rid of my anxiety and depression when I was in the midst of a psychotic break. It's definitely in my top 3 racetams but no, it isn't an antagonist.


[/B]^Asecin, Tianeptine will modulate the AMPA and NMDA glutamate receptors for as the duration of the drug lasts. It would always work on these channels for however long this drug is in your body. It's pharmacology will never change: it will always work on the AMPA and NMDA ionophere.

And tianeptine's effects on the MOR are insignificant on its therapeutic and nootropic effects; you actually need quite large/many times the therapeutic dose to even feel the mu opioid effects. It's serotonergic effects are weak as well. It has much more pronounced effects on dopamine receptors and ionotropic glutamate receptors.

I'm just kind of mad with got stuck with this one. Amineptine would have been better...

Asecin...

I doubt it is because of the glutamate that aniracetam and tianeptine feel familiar too you.

It is more likely due to the fact that both tianeptine and aniracetam both have profound serotonergic and dopaminergic effects in the brain.

"aniractam has POWERFUL sertonergic and dopamiergic effects. this is most likely the cause for the depression" so it will cause rebound depression after stopping it for whatever reason? well, thats not very useful, is it


about tianeptine you say this " It's serotonergic effects are weak as well" but then you say this "It is more likely due to the fact that both tianeptine and aniracetam both have profound serotonergic effect...." so you say it has little value to serotonin but then say it has a lot of value comparison to aniracetam, im confused.

and about its mu opioid effect you seem to think in very high doses it might have such effect which i think again you are unsure of this as i believe i have felt that specific effect at lower standard dosage.

what i want to help figure out and prevent its MOR tolerance and withdrawl, likely "Another long-term adaptation to opioid use can be upregulation of glutamate and other pathways in the brain which can exert an opioid-opposing effect" using something for glutamate modification of sorts?
i really wish to find the best most reliable tolerance and withdrawl MOR prevention pill.

 

[Ligaturd]

My notion that a GABA b antagonist could cause psychosis and excitotoxicity is based off of a misunderstanding of the function of the GABA b receptors, as I assumed a GABA a antagonist would severely impair the brains ability to regulate glutamate levels and cause a syndrome like benzodiazepine discontinuation syndrome. Which it most likely would.

Withdrawal from GABA b agonists causes similar withdrawal to that of GABA a agonists and exhibits neurotoxicity from excitotoxicity due to the down regulation of GABA receptors, effectively removing the brains built in brakes.

So this is based off of mostly assumptions and ignorance.

 

[theGirlWithBlueHair]

GABA B antagonists would presynaptically increase GABA release via presynaptic GABA B receptors as well as decrease subsequent T-type calcium channel activity by blocking postsynaptic GABA B-mediated GIRK-channel activity.

^You are correct in assuming this, but I doubt this would happen in the dosages used as GABA B agonists have been showed to be anticonvulsant in some models of epilepsy, and fasoracetam also induces rapid upregulation of the GABA B receptor as well.

Keep in mind that GABA B agonists can be excitatory and produce kindling effects by inhibiting GABA and activating calcium channels themselves.

And psychoses only results when there is a quite a massive dearth of GABA B receptors in the brain, and I don't think therapeutic levels of fasoracetam can induce this kind of receptor occupancy.

Asecin, sorry about that: when I make posts, I usually have to go back and edit them quite a bit due to the rapidity with which I spit them out and some mistakes I make.

The mu effect can be felt at all dosages; you won't feel typical, strong narcotic effects like you would from say hydrocodone or oxycodone unless it is in higher dosages than the typical prescribed 12.5mg dosage.

I think by saying its serotonergic effects are weak, I was comparing them to other effects, not just saying they are weak in general.

But aniracetam has more serotonergic effects, in my opinion.

I've never gotten rebound depression from aniracetam, but then again I've only ever taken for 3 weeks, and my dose was only 1000mg tid. Do you know of this, personally, by reading about it from case reports?

 

[asecin]

its very hard to find any competent reports on long term usage of any racetam except piracetam, the oldest most used one has probably the vast of research done on. its more like personal experience this one. it kind of lifted depression only to bring it back down with force. i would think its just temporary fix for something more serious and that is all.
on the other hands lots of reports of tolerance and addiction with tianeptine, i keep asking whats the best thing to take during or after use to minimize its tolerance and addiction and so far nothing but i would assume if people would have figured it out they would use same thing for any opiate and be very happy drug users

 

[theGirlWithBlueHair]

During? I dunno. The NMDA antagonists are well known. There is nothing you can take to minimize addiction risk. If you are predisposed to be addicted to opioids, you are going to have that risk regardless.

The D2/D3 partial agonists can somewhat mitigate this effect, but they can also reduce the recreational value.

Interestingly, piracetam and aniracetam have been shown to have GABA B antagonist activity as well, so it might be more common among the racetams:

http://www.ncbi.nlm.nih.gov/pubmed/8801601