How do dissociative drugs deplete the nervous system?

[Solipsis]

I've heard more than once that dissociatves including nitrous but also arylcyclohexylamines can lead to depletion of things like vit B12 and magnesium. Those compounds are involved in ion channels and nervous anatomy, right ... and/or your body's energy household? I started taking CoQ10 and B12 after hearing this and having problems from dissociative use.
Apparently we don't know that much about nitrous but is it a coincidence that it also depletes you of certain biochemicals? Is it the hypoxia only that can lead to neuropathy?

I'm interested to hear more about these types of physiological side-effects from dissociatives, cause I don't understand it one bit.

 

[sekio]

Apparently we don't know that much about nitrous

We actually know quite a bit. It's known that nitrous oxide reacts with and inactivates B12 similarly to how carbon monoxide binds to heme (bids tighter to the active site on the metal atom, preventing the transport of O2 in the case of heme or the use of b12 as a cofactor).

Neuropathy is usually a consequence of chronic N2O use destroying the supply of B12 in nerves/other tissue. To have chronic hypoxia with nitrous use would mean you're constantly breathing it premixed with air or something... not a common usage scenario.

Lots of people get their panties in a knot over N2O causing hypoxia but the fact of the matter is it's not going to kill major amounts of brain cells until you've been breathing it for quite some time and/or exercising heavily while on N2O. Recall that people exercise anaerobically (sprinting etc) and you can, in fact, hold your breath til you turn blue and pass out and regain consciousness spontaneously.

As far as I know arylcyclohexylamines don't deplete B12 or Mg. I think people just encourage use of Mg/Zn to make sure that your NMDA receptors can function properly.

 

[Jonneh]

There are probably also some links with NMDA receptor function. B12 protects against NMDA-induced excitotoxicity (which acts through nitric oxide), and the absence of B12 impairs NMDAR function.

 

[St3ve]

We actually know quite a bit. It's known that nitrous oxide reacts with and inactivates B12 similarly to how carbon monoxide binds to heme (bids tighter to the active site on the metal atom, preventing the transport of O2 in the case of heme or the use of b12 as a cofactor).

I thought the danger with CO was that it made a strong bond to the heme group in red blood cells and could not be removed. The only way to recover would be for the red blood cell to die and get replaced by new ones. If it's the same with NO, repeated use over a few weeks could stack up and cause problems. Might be wrong though...

 

[sekio]

I'm just saying the mechanism of nitrous oxide bonding to B12 is similar to CO bonding to heme, nitrous oxide doesn't actually bond tightly to heme.