From Wikipedia, the free encyclopedia
Jump to: navigation, search

Text removed from Psychedelic drug page, to be edited and added to this page[edit]

The following text was erroneously added to the psychedelic drug page:

Salvia divinorum produces two potent dissociative drugs: The Salvinorins A and B.

^^ Why would you remove that? I'd edit it. Salvinorin A is commonly classed as a dissociative, as it really should be. This section is on dissociatives- drugs that dissociate mind from body. Kappa agonists definitely accomplish this.

The problem with that statement, though, is that Salvinorin B isn't a kappa agonist, isn't an NMDA antagonist and isn't even ACTIVE according to anything I've seen- though as far as I know, no ones' ever looked to see if it has affinity for non-opioid receptors (It'd be interesting to know if it has sigma affinity) (talk) 01:03, 15 July 2008 (UTC) Hammilton

---Dissociatives ([NMDA and PCP receptor agonists/antagonists])---

Ketamine and its parent drug phencylcidine are somatically safe and useful anaesthetics. Ketamine, specially, is used for psychedelic and more general therapeutic purposes (as in the studies by Dr Evgeny Krupitsky of Russia, cited in It´s considered a promising new pharmacological approach to the treatment of chronic alcoholism. Dextromethorphan (DXM), which is a synthetic opioid, has also some hallucinogenic propoerties at doses much higher than those used as cough suppresant, though more possibly it acts through a different mechanism than PCP and ketamine, and it´s also more prone to cause actual neuronal death in a fashion similar to alcohol. It is an uncontrolled substance in much countries, as is usually the case with disagreeable and noxious substances. It is sold Over the Counter in most of the United States. Contrary to dangerous psychotropics or poisonous substances as paraquat, which remain legal, safe psychodelic substances are severly punished by repressive forces, according to the plan for the extinction of certain drugs that the government of the United States enacts since the foundation of the United Nations, specially through the UN´s Bureau of Narcotics. Dangerous or poisonous substances remin uncontrolled, in an world UN´s sponsored effort to make users seeking mind expansion to be intoxicated with substances that deteriorate their minds. The plan of the United States has been denounced as an actual attempt of reducing the recreative drugs available to those that generate serious deleterous addiction (specially brain damage, dementia, or acquired mental retardation) in order to increase the gobernability and submission of the people of the world to the suppliers of the Official American Drugs: Alcohol, tobacco, many pharmaceuticals such as the benzodiazepines.


"though more possibly it acts through a different mechanism than PCP and ketamine, and it´s also more prone to cause actual neuronal death in a fashion similar to alcohol"


Could you cite the research showing that DXM is more likely to cause neuronal death than PCP or ketamine? The only relevant literature I have seen is on DXM as an NMDA antagonist and shows that lower affinity NMDA antagonists are less likely to cause neurotoxic changes in neurons. I realize that Carliss et al. (2007) and Ortiz (1999) discuss different drugs, but I have formulated a hypothesis to explain their apparently contradictory reports. Olney et al. (1989) showed that weaker NMDA antagonists reverse the neurotoxic changes in neurons more quickly than more powerful NMDA antagonists. For example, high doses of PCP caused vacuoles to be visible for upto a day later, while ketamine - a weaker antagonist - produced vacuoles which reversed more quickly. Ortiz et al. (1999) report that DXO caused neurotoxic changed which were observed half an hour after drug administration. Carliss et al. (2007) reported no neurotoxic changes due to DXM administration 24 to 48 hours later. I believe that the following simple hypothesis is consistent with the facts: DXM metabolism produces the NMDA antagonist DXO, which does produce neurotoxic changes, consistent with Ortiz et al. (1999). However, due to the relatively weak NMDA antagonist of DXO, these changes are more quickly reversible and are not visible after 24 hours.

Carliss RD, Radovsky A, Chengelis CP, O'Neill TP, Shuey DL. (2007) Oral administration of dextromethorphan does not produce neuronal vacuolation in the rat brain. Neurotoxicology. 28: 813 - 818. Olney JW, Labruyere J, Price MT. (1989) Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs. Science. 244: 1360 - 1362. Olney JW, Labruyere J, Wang G, Wozniak DF, Price MT, Sesma MA. (1991) NMDA antagonist neurotoxicity: mechanism and prevention. Science. 254: 1515 - 1518. Ortiz GG, Guerrero JM, Reiter RJ, Poeggeler BH, Bitzer-Quintero OK, Feria-Velasco A. (1999) Neurotoxicity of dextrorphan. Arch Med Res. 30: 125 - 127.


Nitrous Oxide[edit]

From the page Effects of nitrous oxide on the body, "It (N2O) inhibits the NMDA receptor at partial pressures similar to those used in general anaesthesia (Jevtovic-Todorovic et al., 1998; Mennerick et al., 1998; Yamakura & Harris, 2000)." Therefore, I think that N2O should not be classified as an inhalant (which merely discribes its method of intake) and move it under NMDA Receptor Antagonists. I'll move this but I'm open to discussion if anyone believes otherwise.

Also, this opens the possibility of N2O causing Olney's Lesions. However, it is possible that it does not cause cellular vacuolization because of its effect on the GABA receptor (and inhibiting the GABA receptor helps prevent vacuolization.) Either way, I'd like someone more qualified than me to verify both my changing of its classification and the possibility of Olney's Lesions. Jolb 23:25, 16 January 2007 (UTC)

^ Agreed on Nitrous not being a true inhalant- it has none of the dangers they do (besides total suffocation if you're stupid). However, the idea that nitrous oxide may cause olney's lesions in humans is baseless. Even long term PCP and ketamine addicts have never presented with an olney's lesions. Never been seen in humans, not once. Olney himself as admitted that he jumped the gun on the issue. —Preceding unsigned comment added by (talk) 01:08, 15 July 2008 (UTC)

First paragraph of introduction[edit]

Paragraph cites no sources and seems based entirely on the subjective experience of the person who wrote it. I recommend it either be removed or find sources to support the claims. —Preceding unsigned comment added by PhishHeadSCI (talkcontribs) 03:04, 23 October 2008 (UTC)

I have a hard time accepting that the first reference given actually supports the claim it's used to support (i.e. that dissociatives block signals to the conscious mind from other parts of the brain). First of all, the article wasn't cited properly and the part of the title just before "in rat brain ..." was left out of the cited tilted. I sincerely doubt that an article on how PCP changes glucose utilization in the rat brain is supposed to support the initial sentence. The second sentence is just poorly written and I don't consider it accurate. Which other drugs produce such action? As far as I'm aware, "blocking signals to the conscious mind from other parts of the brain" is a characteristic effect of dissociative drugs (though I really dislike how its phrased). Overall, the article isn't very good. I re-wrote some of the section n effects because it made the typical mistake of trying to compare dissociatives to LSD and psilocin. I *DO* think they can be compared as they do alter largely the same mental functions and areas of perception, only in different manners. I just think that starting off the effects section by comparing to LSD and psilocin give those drugs a status as the norm and can impact the way we talk about dissociatives. AlkaloidMan (talk) 10:22, 23 October 2010 (UTC) AlkaloidMan

Acetylcholine-inhibitor dissociatives[edit]

In the first line of Deliriant article it says "The deliriants (or anticholinergics) are a special class of acetylcholine-inhibitor dissociatives." So are deliriants a sort of subclass of dissociatives and if they are should they be mentioned in this article? --Ahabvihrea (talk) 18:40, 27 November 2008 (UTC)

Yes, they should be mentioned with a See deliriants link. They have their own article because while they are a sort of dissociative, they are in a class of their own. --Thoric (talk) 16:52, 10 February 2009 (UTC)
How are deliriants dissociative? I've never heard of or experienced dissociative effects(sensory deprivation for example) from deliriants. Just delirium. YVNP (talk) 03:04, 5 November 2009 (UTC)


Is Dextromethorphan an uncompetitive channel blockers? —Preceding unsigned comment added by (talk) 13:26, 10 February 2009 (UTC)

Yes. All of the most common NMDA antagonists are uncompetitive, though this is a mater for the NMDA antagonist article. (talk) 16:21, 8 October 2009 (UTC)

Dissociatives aren't hallucinogens?[edit]

"Hallucinations from these dissociatives are generally only experienced in dark rooms or with eyes closed, unless at very high doses above what is normally consumed recreationally" I've taken DXM at doses of 300(which is quite a rather low recreational dose) and experienced CEVs and visual distortion(everything turned choppy and colors were much brighter). I've also read on Erowid and it seems DXM does indeed have visual effects. This statement seems to be suggesting dissociatives are not "real" drugs and therefore can't possibly make you hallucinate. removed YVNP (talk) 03:02, 5 November 2009 (UTC)

In my opinion, dissociatives could be called "dissociative hallucinogens." Their hallucinogenic effect is well documented and they're even referred to as "hallucinogens", "psychodysleptics", "psychedelic" (e.g. you can find plenty of references to "ketamine psychedelic therapy"), and "psychotomimetic." I have heard some try to argue that NMDA antagonists / dissociative anesthetics are not "true" hallucinogens, but I have never seen any sort of justification for this, especially since you can find these drugs referred to as "hallucinogens" (and their equivalent names) in scientific literature. As for the quote above about hallucinations, I would say that depends on what the person considers a "normal" dose. AlkaloidMan (talk) 10:19, 23 October 2010 (UTC)AlkaloidMan

Wouldn't it be better to put κ-opioid receptor agonists in a different group?[edit]

I think most people would agree that Ketamine (a NMDA receptor antagonist) and Salvia Divinorum (a κ-opioid receptor agonist) have quite different psychological effects. Wouldn't it be better to put κ-opioid receptor agonists into a group called dysphoriants?Zanthius (talk) 16:40, 1 March 2015 (UTC)

Unsourced, WP:NOTCATALOG[edit]

The content below is almost entirely unsourced and has degenerated into an indiscriminate list of compounds that fall into various categories.

I moved it here per WP:PRESERVE. Per WP:BURDEN please do not restore without finding independent, reliable sources, checking the content against them, and citing them, and ensuring that this content has appropriate WP:WEIGHT in the article overall. Not at all sure that this list cluster belongs anywhere tho.

NMDA receptor antagonists
κ-opioid receptor agonists


  1. ^ Giannini, A. James; Underwood, Ned A.; Condon, Maggie (2000). "Acute Ketamine Intoxication Treated by Haloperidol". American Journal of Therapeutics. 7 (6): 389–91. PMID 11304647. doi:10.1097/00045391-200007060-00008. 
  2. ^ Giannini, A. James; Giannini, Matthew C.; Price, William A. (1984). "Antidotal Strategies in Phencyclidine Intoxication". The International Journal of Psychiatry in Medicine. 14 (4): 315–21. doi:10.2190/KKAW-PWGF-W7RQ-23GN. 
  3. ^ Giannini, A. James; Price, William A.; Loiselle, Robert H.; Malone, Donald W. (1985). "Treatment of Phenylcyclohexylpyrrolidine (Php) Psychosis with Haloperidol". Clinical Toxicology. 23 (2-3): 185–9. PMID 4057312. doi:10.3109/15563658508990627. 
  4. ^ Tarter, RE; Ammerman, RT; Ott, PJ (1998). Handbook of Substance Abuse: Neurobaehavioral Pharmacology. NY: Plenum Press. p. 265. ISBN 0-306-45884-5. 

-- Jytdog (talk) 00:52, 31 July 2017 (UTC)