Talk:Ketamine

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

There's evidence of addiction and toxic effects from telemedicine prescriptions of ketamine in the US. [1]https://www.nytimes.com/2023/02/20/us/ketamine-telemedicine.html?smid=url-share Neiabr (talk) 18:32, 25 February 2023 (UTC)

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)

Including role of glutamate in antidepressant effects

Currently, under the "Mechanism of action," the article states: "In any case, it has been elucidated that acute blockade of NMDA receptors in the brain results in an activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPA receptors), which in turn modulate a variety of downstream signaling pathways to influence neurotransmission in the limbic system and mediate antidepressant effects of NMDA receptor antagonists like ketamine." The article does not address why the acute blockade of NMDA receptors in the brain results in an activation of AMPA receptors, which is very important to the explanation. The most accepted explanation of this appears to be due to a "glutamate surge".

This except explains it well: "Subanesthetic-dose ketamine administration leads to immediate presynaptic disinhibition of glutamatergic neurons, producing a glutamate surge (Moghaddam et al., 1997). This surge is thought to result from the blockade of NMDA receptors targeting γ-aminobutyric acid-ergic interneurons, leading to local inhibition of interneuron tonic firing and subsequent disinhibition of glutamate transmission (Homayoun and Moghaddam, 2007). Due to a blockade of NMDA receptors on postsynaptic excitatory neurons, excess synaptic glutamate is primarily taken up by AMPA receptors, thereby activating neuroplasticity-related signaling pathways (including mammalian target of rapamycin complex 1 (Li et al., 2010; Li et al., 2011) and brain-derived neurotrophic factor (Liu et al., 2012), both of which result in increased synaptogenesis and synaptic potentiation)."

I am thinking that the sentence should be changed to something to the effect of: "In any case, it has been elucidated that acute blockade of NMDA receptors in the brain results in an increase in glutamate production, which leads to an activation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPA receptors), which in turn modulate a variety of downstream signaling pathways to influence neurotransmission in the limbic system and mediate antidepressant effects of NMDA receptor antagonists like ketamine." Wikipedialuva (talk) 08:31, 11 October 2023 (UTC)

Agreed, please change. 2001:9E8:4629:A400:F5BF:1E33:500D:E6E2 (talk) 21:02, 17 December 2023 (UTC)

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

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)

Do you have a reliable source the indicates that is another name for ketamine? OhNoitsJamie ^Talk 15:58, 5 November 2024 (UTC)

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)

Public confusion about clinincal benefit vs long term safety

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)

Are there WP:MEDRS sources for this? Bon courage (talk) 10:16, 19 May 2025 (UTC)

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)