Can't really awnser your question about NMDA antagonists but here something that can shed light about the relation of psychedelics and genetic downstream regulation:
The first step in a complex signalling system involves the binding of specific ligands (LSD, psilocin, DMT…) at the cell surface to a G Protein Coupled Receptor, thereby activating the receptor. The signal is transmitted into the cell via a conformational change in the receptor, which results in the activation of the bound G protein. GPCRs act as guanine nucleotide exchange factors for the a subunit of the G protein, whereby activated receptor promotes the exchange of bound GDP (guanine diphosphate) for Guanine Tri Phosphate on the a subunit, which is the rate-limiting step in G protein activation. The binding of GTP changes the conformation of ‘switch’ regions within the a subunit, which allows the bound trimeric G protein (inactive) to be released from the receptor, and to dissociate into active a subunit (GTP-bound) and bg dimer. The a subunit and the bg dimer go on to activate distinct downstream effectors, such as adenylyl cyclase, phosphodiesterases, phospholipase C,
Src, and ion channels. These effectors in turn regulate the intracellular concentrations of secondary messengers, such as cAMP, cGMP, diacylglycerol, IP3, DAG, arachidonic acid, sodium, potassium or calcium cations, which ultimately lead to a physiological response, usually via the downstream regulation of gene transcription. The cycle is completed by the hydrolysis of a subunit-bound GTP to GDP, resulting in the re-association of the a and bg subunits and their binding to the receptor, which terminates the signal.
I hope this is not overly technical...
