For an acute burst of cognitive function, try the NMDA trio of D-Serine, sarcosine, and DAA along with a potentially synergistic AMPA-based agent: aniracetam.
Can D-Serine, itself, activate the NMDA receptor? Wouldn't a cascade of effects like--preceding agonism of the AMPA receptor, membrane depolarization, NMDA magnesium displacement, and accompanying binding with glutamate--need to be met prior to agonism?
So, D-Serine is "limited" by prior AMPA activation (among other criteria)? Could it still lead to over activation of the NMDA receptor? I guess this is something that everyone worries about when messing with the NMDA receptor?
Now, what about allosterism? So, piracetam (and others) don't directly activate any receptor, but it modulates glutaminergic receptors through allosteric activation. Now, aniracetam has a high affinity binding to the AMPA receptor. Will modulating the AMPA receptor lead to over-activation of the NMDA receptor?
Alright, I was pretty long winded, but I needed to work through that post to help myself understand.
So, hypothetically speaking, is it safer (avoiding NMDA excitotoxicity) to modulate the AMPA receptor through the use of -racetams, or to activate the NMDA receptor through the use of D-Serine (and follow the cascade of preceding criteria prior to agonism of the NMDA receptor)?