I'm not ashamed to say you are absolutely right about the etymology of narcotics.
I also did some more research on the stuff mentioned previously (before reading your post actually), since I was also wondering if my explanation was correct or not.
I found a textbook reference for the toxicological definition of narcosis
HERE.
Turns out that sometimes you can better use Google than PubMed.

As you can see this edition is a publication from 2004, so it was not some ancient misunderstanding about the MOA of narcotics.
Again, not true. The term was applied to all of these drugs that produced a numbed, stuporous state. I'd have to look around, but I'd be surprised if ethanol wasn't described as a narcotic long before our modern anaesthesia was even developed.
I think the truth lies somewhere in the middle here...
If you look at the
American legal definition of narcotics, I believe it is limited to all opiates/opioids and cocaine.
But there is possibly also a pharmacological definition, though I wouldn't be surprised if the term 'narcotic' is somewhat outdated, just like antipsychotics are now usually called neuroleptics.
Haha, must say you got me on the Imperial system.
But then again...the Americans were stupid enough to keep it after they kicked the British out.
You apparently believed that volatile anaesthetics like chloroform didn't bind to receptors!
It was never my intention to say that they do not bind to receptors.
I am very aware they bind to receptors, receptors are proteins after all and fi chloroform is widely used for the precipitation of proteins.
I just don't think that the main effect of inhaling solvents is produced by interaction with a receptor.
Of course there will be a few exceptions, but if you try to look at it through the above definition of narcosis, perhaps you'll understand what I mean.
All solvent cause this narcosis, because they are by nature highly soluble in the lipid bilayer.
So I made a list of a few well-known solvent, but if chloroform merely acts by recepter interaction I must say I wasn't aware of that.
But looks to me like it's a combination between narcosis, starting at threshold levels, and receptor activation/inhibition when concentrations are high enough.
we're talking about how chemicals interact with receptors
You (plural) were talking about how chemical interact with receptors.
I, on the other hand, was talking about how chemicals interact with the cell membrane.
Perhaps that's part of the mutual misunderstanding here?
I don't see how this developed from what came before it, it doesn't seem relevant at all.
It was more a general frustration towards the excessive labeling of chemicals (mostly by governmental agencies).
Something is a narcotic or a class XYZ drug.
I think it's bullshit, something is a partial 5HT2C-agonist or an inverse NMDA-agonist.
You should not group chemicals because they all cause your skin to turn blue (for instance), but you
could group all chemicals that cause pain relieve because they interact with a subtype of opiate receptor.
Luckily, this change is already in progress in pharmaceutical science, where most drugs are classified by their receptor affinity.
BTW, I wonder what your definition of 'mode of action' is, because my definition of MOA is the whole array of receptors that are influenced by a compound.
Classification of chemicals based on structural relationships is more logical from a physicochemical point of view.
But pharmacologically speaking I think receptor affinities should get more attention than structural relationships.
