displaced?
What this table demonstrates is that DXM binds to four separate places, two with high affinity. The first binding site is almost certainly the sigma1 receptor (see <5.2>). The second site is probably the PCP2 receptor (see <5.4>), and the third site is probably the sigma2 receptor. The identity of the fourth site is still up for grabs but is probably the NMDA channel PCP1 site (see <5.3>). Because DXM has been found to bind with Na+ and Ca2+ channels at low affinity (59), (see <5.5>), there may be a fifth binding site. Most of the “stoning” or intoxicating effects of DXM are likely due to NMDA receptor blockade. Alcohol’s intoxicant effect seems to be mediated in part by NMDA receptor blockade (its depressant effect is due to GABA activity; DXM has no activity at GABA receptors) (28,61,62). The dissociative anaesthesia of high DXM doses is also likely due to NMDA receptor blockade (63). The disruption of sensory processing is probably a combination of NMDA blockade and sigma activation