N&PD Moderators: Skorpio | thegreenhand
Cerebrocortical GABAergic neurons in the posterior cingulate and retrosplenial cortex get disinhibited in respons to NMDA blockade. And that in turn leads to an excessive release of acetylcholine leading to excitotoxicity.
NMDA antagonist neurotoxicity(NAN) is reduced by GABAergic agents, mAChr antagonists and alpha2-adrenergic agonists.
Galantamine on the other hand is expected to increase NAN.
That's a really interesting question indeed. If the acute effects of a dissociative are overly relieving, and chronic use of such one leads to a quasi-permanent state of the former, so this could really make sense ....... but there are all the papers about schizophrenia models based on ketamine and PCP. Then again, they use healthy rodents to try this on, and when I presume to have some weird opposite-of-schizo genetics, well ... no clue, but interesting.Does that also imply it's possible that via that way one may therapeutically prune those neurons if they are one of the causes of dysfunction or a disorder? The ethics of forms of chemical lobotomy are another matter of course... Or the price to pay for what sounds like chronic or permanent desensitization.