Granted, this isn't endogenous in everybody (just as well)
But, hows about NMDAr autoantibodies? anti-NMDAR-encephalitis is an interesting condition. Typically presents as a severe, but eminently treatable encephalitis, showing a very pronounced subset of dissociative symptoms, including psychosis, delirium, dissociation, anxiety, hallucination/delusions, along with seizures.
IIRC its for some reason often comorbid with an ovarian teratoma being present in females (although this is not by any means to be considered pathognomonic), and seems in many cases to resolve, or rapidly become more responsive to therapy (which includes corticosteroids, immunosuppressants and/or other immunomodulatory agents). Therapeutic prognosis appears relatively positive in the short term, higher immunostaining reactivity of autoantibodies directed at NMDAr subunits, from a few papers I flicked through online earlier whilst bored out of my mind, waiting for the pharmacy to open and my rx to arrive., appears to be associated with a worse prognosis short- and long-term, taking longterm deficits in neurological function into account. And a common target seems to be NR21 subunit, which forms the NMDAr glycine allosteric binding site.
Isn't the active compound in the psychotropic mulberry species (forget if it is the white, or black), deoxyjirinomycin, isn't that one an NMDA antagonist?
Alternatively there are some (although not to my knowledge, dissociative) compounds acting as NMDAr antagonists in cat's claw (Uncaria tormentosa), IIRC. Might be mistaken there though. And some spider toxins, such as jorotoxin act at the polyamine regulatory site.
) (I don't think that magnesium really counts, as it simply modulates flows through ion channels).
