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Talk:Ketamine

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DateProcessResult
September 1, 2009Peer reviewReviewed

Article on the impact and concerns of enabling legal tele-medicine ketamine prescriptions

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There's evidence of addiction and toxic effects from telemedicine prescriptions of ketamine in the US. https://www.nytimes.com/2023/02/20/us/ketamine-telemedicine.html?smid=url-share Neiabr (talk) 18:32, 25 February 2023 (UTC)Reply

NYT is fully paywalled so it might as well not exist. Even closed-access journals provide abstracts. NYtimes isn't a reliable medical source, anyway. A Shortfall Of Gravitas (talk) 05:39, 26 April 2025 (UTC)Reply

Long form chemical name of Ketamine (2-Cl-2’-oxo-PCM)

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I think the long form chemical name of Ketamine (2-Cl-2’-oxo-PCM) should be added to the article. Who else has been looking for this information but can not find it? Daimontoppi (talk) 15:44, 5 November 2024 (UTC)Reply

Do you have a reliable source the indicates that is another name for ketamine? OhNoitsJamie Talk 15:58, 5 November 2024 (UTC)Reply
Nobody, because that's not the "long form" name. That's a weird abbreviation research chemical people came up with so they could look like they knew what they were doing as far as I can tell. All the instances in a search are forum posts from somewhere in eastern Europe and a thread on reddit asking if that should be the name of it. Ketamine variants are named using an etamine postfix with modified abbreviations for things like methoxetamine / methoxmetamine / ethketamine etc except when the chlorine atom is replaced and then you get things like 2-fluorodeschloroketamine. As soon as the cyclohexyl ring is replaced with a cyclohexanone the PCP style abbreviations aren't generally used anymore. A Shortfall Of Gravitas (talk) 06:43, 26 April 2025 (UTC)Reply

Public confusion about clinincal benefit vs long term safety

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A number of primary sources document permanent brain changes due to Ketamine use such as cell death and elimination of branch points in the dendrite arbor, also atrophy of various parts of the brain.


For treating depression (where alternative treatments include removal of part of the brain by surgery, or electroconvulsive therapy), a permanent change to the brain could be a very beneficial palliative choice.


My worry is that there may be a misunderstanding to the effect that the fact a substance has a meaningful palliative benefit for a condition like depression could get confused with a notion that Ketamine is a 'designer drug' which 'improves' cognition unconditionally among those who are in the know.


Therefore I hope someone can include a section about structural damage to the brain which Ketamine causes, and a balanced discussion about how such damage can be considered acceptable for palliative applications.Createangelos (talk) 10:14, 19 May 2025 (UTC)Reply

Are there WP:MEDRS sources for this? Bon courage (talk) 10:16, 19 May 2025 (UTC)Reply
Although the refs are a bit too primary (as you correctly caution about) I have had a go with this myself, not great and I'd invite more competent editors to fix my mess. I moved the sentence about cognitive deficits and delusions seen in frequent recreational users into a new section and included one NIH review article about reduction of white and grey matter and observed atrophy and a science direct about the concern with frequent repeated low doses regarding dendrite trees. Maybe I am too much using primary sources? NIH is sort-of a nice secondary source (I hope) until someone finds something better? I don't want to be pov however I worry that the article could be miseading if people don't make a distinction between beneficial medical uses of planned coures of therapy versus ongoing recreational use based on a designer notion that doctors proved it improves the brain. Createangelos (talk) 14:38, 19 May 2025 (UTC)Reply

Incorrect Pharmacology Data

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The article mentions that Ketamine is a μ-opioid receptor antagonist with a Ki of 42, however, this is incorrect. Ketamine acts as a weak μ-opioid receptor partial agonist, however, the extent to which these receptors contribute to ketamine's in vivo pharmacology is unknown. In 2018, a small clinical trial by Stanford Medicine researchers found that ketamine's antidepressant effects could be suppressed by first giving patients naltrexone, a μ-opioid receptor antagonist.


https://pubmed.ncbi.nlm.nih.gov/36841701/

https://pmc.ncbi.nlm.nih.gov/articles/PMC6395554/

https://med.stanford.edu/news/all-news/2024/02/ketamine-sex-opioid.html ~2026-14987-21 (talk) 12:45, 1 May 2026 (UTC)Reply

Wiki Education assignment: Molecular Neuropharmacology

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This article is currently the subject of a Wiki Education Foundation–supported course assignment, between 24 August 2026 and 7 December 2026. Further details are available on the course page. Student editor(s): DeepaSubramanya21 (article contribs).

— Assignment last updated by Eleni Anni (talk) 16:24, 28 September 2026 (UTC)Reply