I was reading up on the 3-MeO-PCP wiki expecting that my SO who is not well versed in this stuff might check out soon...
It mentions that the substance is despite popular belief mostly a selective NMDA antagonist.
This raises so many questions: the mania and lack of or rather high threshold for anaesthesia were, I thought, explained by action on DAT remotely comparable perhaps of pipradrol deriv related side effects.
If not, then why do some dissociatives produce much more anaesthetic action (I thought it was pretty intrinsic to NMDA antagonists)? So much more that it determines what effects can be enjoyed while remaining functional or cogent?
In pure NMDAAs what is unavoidable primarily? Amnesia looking at dizolcipine/ diphenidines..?
Its hard to get a grasp of how these qualities link together..
Do you suppose it depends on where in the brain there is NMDA antagonism taking place or how selective or local that is? For example how strongly the cerebellum is affected in relationship to dosage ranges?
It mentions that the substance is despite popular belief mostly a selective NMDA antagonist.
This raises so many questions: the mania and lack of or rather high threshold for anaesthesia were, I thought, explained by action on DAT remotely comparable perhaps of pipradrol deriv related side effects.
If not, then why do some dissociatives produce much more anaesthetic action (I thought it was pretty intrinsic to NMDA antagonists)? So much more that it determines what effects can be enjoyed while remaining functional or cogent?
In pure NMDAAs what is unavoidable primarily? Amnesia looking at dizolcipine/ diphenidines..?
Its hard to get a grasp of how these qualities link together..
Do you suppose it depends on where in the brain there is NMDA antagonism taking place or how selective or local that is? For example how strongly the cerebellum is affected in relationship to dosage ranges?
