As you well may know , tianeptine is one of the most potent nootropics (if not the most) out there. It has several mechanisms : it potentates AMPA and NDMA (excitotoxicity?) in CA1 region, it modulates glutamate and currents of NMDA-AMPA and the rest in other regions(protects against stress), it is a full opioid MOR agonist and a full DOR agonist (with much lower potency) and increases BDNF. Also ,sadly , lowers acetylcholine at high doses.
A friend of mine started using tianeptine for depression , GAD and SAD about 5 months ago, at normal 12.5x3/day dosage. From the first week his depression almost totally lifted.
He also used it recreationally (about 2-4 times a week) at: 12.5-37.5-12.5/day. After the 37.5 dose (that was taken once a day 2-4 times a week) we would feel tired/sleepy, angry/irritable , mentally slow/misusing words/brain fog for a few hours after.
After a while he started using that recreational regiment every other day (one day 12.5x3(nromal),one day 12.5-37.5-12.5). He noticed his depression totally went away, his anxiety lowered, cognitive capacities sharply increase, positive outlook and social/good mood. The acute effects of 37.5 remained (angry,slow mentally,tired/sleepy). This was two months after starting.
He also added buspar to further lower anxiety. This would last only 2.5 days because of side effects (sleepy and slight involuntary movements-tianeptine enhances D2 receptors , amongst others, and buspar acts on them as an antagonist). Also on buspar, tianeptine would be greatly reduced, so he took a tolerance break (only taking normal doses) for about 1.5 weeks.
After this, when he used it recreationally the effects were less intense and he would get slight involuntary movements that would go away with normal doses. After the break he would use recreationally about 2-4 times a week, but after a while he started using it in this fashion every other day.
He would become angry/irritable the next day after recreational use, also in this fashion his previous slight akathasia/RLS from tianeptine became progressively worse until it would become unbearable 3 months later.
He also used a few times 50 instead of the regular 37.5 , and took it a few times with benzos - the effects the next day were much worse in this fashion - the acute effects - irritable/tired/sleepy/angry/mentally slow/missusing words would last into the next day and he would be cognitively impaired for a day.
In the above mentioned 3 months, he noticed a very,very sharp cognitive increase (that reflected in his programming and grades) , a sharp decrease in anxiety, depression was totally gone, mood was great, social anxiety took a sharp decline and life was better than ever.
At the end of the aforementioned 3 months he had his usual regiment : one day normal (3x12.5) , one day (12.5,37.5 or 50,12.5) , this went on for about a week.
After that time, i heard him snore loudly a few times , also had a very slight breathing problem during the day. He slowly tapered off in this fashion, while keeping normal dosage (first 37.5 every other day , then 37.5 after one day pause, then after 2 days pause, then after 3, then after 4.
But, what made him taper was this : at the end of those 3 months something BIG happened. His anxiety was almost non-existent, his depression the same, BUT his cognitive abilities took a BIG hit, almost instantly, he was much lower than before starting tianeptine(could not reason complex problems,had very much memory problems, verbal fluency was much lower, he was much slower mentally also sleepy during the day (2.5 hours after normal dose) and lethargic, his akathasia/RLS became unbearable. After that he would only use recreationally once every 5 days, in the rest of days , normal doses.
3 weeks after those 3 months, the cognitive effects have not gone away, and the akathasia/RLS became unbearable. So he decided to stop tianeptine entierly. Started tapering to 2x12.5 mg a day.
What could cause these effects?
I have read that tianeptiene potentates AMPA and NMDA in CA1, could that be it? Excitotoxicity? I think so, he once took piracetam with tianeptine , and it made the akathasia/RLS 3x worse. Piracetam acts on AMPA and acetylcholine, and acetylcholine would not cause this.
Will this be permanent? What could have caused this and why? Is there something available to repair excitotoxicity damage ? (if that is what caused it)?
Could this be excitotoxicity?acetylcholine deficiency? It was shown to reduce acetylcholine by 40% , but only in rats and at very high doses 30mg/kg. What would be the human equivalent dose to that? Anyway acetylcholine deficiency has a simple cure, but i doubt that's it. Could it be a form an opioid withdrawal? I highly doublt that, he can take days long break with normal dosage. Could it be trkB downregulation (receptor for BDNF), killing brain cells?
Last question : what would those higher doses do in modulating AMPA/NMDA in brain regions (lower them/up them)? Also i don't need to ask about CA1 region because that would potentate AMPA and NMDA even further there.
"Tianeptine reduces N-methyl-D-aspartate (NMDA)-receptor-mediated synaptic currents, without affecting a-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) currents, in LA neurons. By contrast, tianeptine enhances both NMDA and AMPA currents in area CA1"
UPDATE: He tapered too quick, got involuntary movements while sleeping and some other weird stuff, along with bad mood and brain fog. He will taper slower.
Edited by Tianeptine236, 18 April 2015 - 02:32 PM.
