Ketamine is indeed an SNRI but I don't think its quite as much of an SNRI as DXM and not as promiscuous at other sites like Sigma 1 receptor. This is in comparison to DXM which works to suppress cough at very low doses via effects on Sigma1. I'm not 100% sure exactly what targets contribute to DXM's subjective "dirtyness" but I don't think that those anecdotal reports are invalid.
There are certainly differences between the NMDA antagonists that have a lot to do with their binding proclivities. PCP can be a tad more psychotomimetic and its possible that this is due to its direct effects on dopamine which other NMDA antagonists may not share.
Ketamine can be used as an anesthetic in emergency situations specifically because it is safe in terms of physical safety (neurogenic bladder risk should be extremely minimal in a one-off use).
But you won't see ER physicians giving people DXM for anesthesia for a few reasons. For starters the intense NRI can low the seizure threshold. There are the liver enzyme/metabolism issues. It can induce intense itching/histamine release in some people. It could be hard on the liver itself, especially for people stabilized on other medications that need to be kept in a narrow concentration range (anti-epileptics). It could be more likely to produce adverse psychiatric effects in the short term, although lord knows all NMDA antagonists can cause psychiatric side effects in the long term. Oftentimes elderly patients have a hard time recovering from anesthesia with normal anesthetics.
Memantine has glutamatergic activity? You're referring to effects on glutamate receptors other than NMDA? Blocking NMDA receptors leads to downstream glutamate release yes, but I don't believe its similar to ketamine with regards to hydroxynorketamine and the effects on AMPA receptors. I'm personally not aware of other glutamatergic effects.
I'm not saying the effects on nicotinic acetylcholine receptors don't help shape the subjective effects, nor the effects on 5-HT3 receptors, but that and NMDA antagonism may be all that memantine appreciably has going for it and thats certainly a whole lot less than DXM has.
Its very likely that memantine isn't an appreciable agonist at D2 receptors. There is a researcher Philip Seeman who loves to report D2 agonism with every drug on the planet, even when its probably not there. There are many incidences where Seeman reports D2 agonism/partial agonism and another lab can't confirm the results. I'm pretty sure the PDSP's screening showed memantine's D2 affinity was >10,000 Ki.
Activity at Sigma1R plays some role in memantine's (most ligands really) effects but its probably not as appreciable as DXM's sigma agonism. Even if the affinity/occupancy of Sigma1R is the same between DXM and memantine, we still have the issue of intrinsic efficacy. Sigma1R agonism might also be a bit context dependent in the sense that Sigma1R agonism related effects express themselves differently depending on the basal activity of the brain.
I see now what wiki wrote regarding Memantine/Sigma1R - "
It acts as an agonist at the σ1 receptor with a low Ki of 2.6 µm (2600 nm).[23] The consequences of this activity are unclear (as the role of sigma receptors in general is not yet that well understood) and memantine is probably too weak at the sigma binding site to exhibit significant agonist effects, only exhibiting partial agonism or antagonism. Some of memantine's adverse effects arise through this route."
My hunch is that the potent reuptake inhibition effects, effects at Sigma1R and histamine related effects can explain in part the "dirtyness" of DXM. When compared to something like memantine, I personally think that memantine feels subjectively much "cleaner" - In my experience you can tell what is the NMDA antagonism and what is missing compared to DXM - the almost psychotomimetic/"brain fry" portion of DXM.
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NMDA antagonism by itself without the other stimulatory effects is actually quite boring and an experience that usually isn't worth trying. That is of course my own subjective intuition and it should be taken as such."
It is indeed generally the case that NMDA antagonists with reuptake inhibition are more abuseable.