Posted 19 November 2009 - 10:09 AM
IMHO, tianeptine pretty much epitomizes the definition of an "atypical" antidepressant when it comes to its mechanism of action.
often you'll find, unfortunately, that the atypical antidepressants never have a fully understood mechanism of action --> bupropion and tianeptine certainly make good examples of this kinda situation.
reading the patent's literature, it seems to suggest that tianeptine somehow prevents the hype-ractivation by glutamate without having any sort of direct antagonistic effect on the NMDA receptors. wow. okay, after reading that, i am officially intrigued. i'll probably dig into that later.
anyway...
here's a general, simplified joe-shmoe rundown of your AMPA and NMDA receptors and how tianeptine and piracetam appear to affect them:
so, first we have our AMPA receptors. once the AMPA receptor opens up, ions flow into it and start charging it. there are several different ion types that'll flow in, but the main one of concern is calcium. the AMPA receptor "fires" (aka polarizes) when the ions flowing through it charge it up to a certain threshold. once it fires, it closes up again. when your AMPAs fire, they sprout other little AMPA buddies nearby.
next, we have our NMDA receptors. we need both of these bad boys to induce long-term-potentiation, which essentially means the neuron has been "strengthened" so that it fires off just as strong with a lower amount of neurotransmitter stimulation. the NMDA receptor naturally has a magnesium "front door" or sorts blocking ions from flowing in, which is where AMPAs step in. the charge from maybe one AMPA receptor probably won't be enough to open up NMDA receptor, but after enough AMPA receptors form around the NMDA from their firing, eventually, their collective charge will be enough to knock out the magnesium blocking the way. once the magnesium is out of the way, then ions can flow through the NMDA receptor.
glutamate is the main handyman with all of this, and it does a pretty good job of prying open [aka exciting] those AMPA receptors and will get you to the front door on the NMDA receptor. now obviously, the AMPA receptors can't just stay open for ions to rush through all the time and will close once they fire, but that certainly doesn't affect whether or not glutamate will just open it up again when it can. THIS is where we get neurotoxicity. once your glutamate starts running around and partying in your brain, it'll start opening up your AMPAs more than you can handle, and more and more calcium will flow through. once you've had too much calcium flow through: poof. your neuron is zapped. gone.
so when you read something being called a "modulator," it's basically describing it's action on the receptor. what the patent that you posted basically says is that taking tianeptine is kind of like putting a really scary, shaved head, muscle-bound bouncer/doorman in front of your AMPA receptors. this way, if your glutamate gets out of hand and wants to start crashing parties in your AMPA receptors, your buddy tianeptine will be there, ready and waiting for it at the door armed with a resounding "shove off" and a nice, beefy pair of crossed arms.
piracetam on the other hand, i guess, is described as a "positive modulator." what this basically means is that, instead of tianeptine putting it's mr-universe-with-a-bad-attitude doorman at the front of your AMPA receptor party, taking piracetam is like putting a nice, friendly doorman out front who happens to be best buddies with glutamate and will let him in once the boss isn't looking.
so i guess, in theory, there could be an interaction. again, IN THEORY, it could be a bit like having both of your doormen out front when glutamate comes around --> in that, they might not exactly come to an agreement once glutamate starts knocking.
-
like x 1
