N&PD Moderators: Skorpio
Potency of ketamine versus dextromethorphan as an NDMA antagonist?
JohnBoy2000
Bluelighter
Both used as dissociatives.
I believe ketamine used more frequently, but there is a claim that dextromethorphan is potent in this capacity also.
Do people really experience dissociation from too much cough medicine??
Cotcha Yankinov
Bluelight Crew
People absolutely experience dissociation from ingesting DXM, but its the metabolite DXO that is the NMDA antagonist.
There are differences between all the different NMDA antagonist though, both because of off target effects (sigma/NRI in the case of DXM/DXO) and differences in how they block the NMDA channel. Some NMDA antagonists are "high trapping" (ketamine) and really sit in the channel for a long time and then others are low trapping, like memantine, which goes in and out of the channel quickly.
Limpet_Chicken
Bluelighter
At least some low-trapping antagonists at NMDARs are still able to perform as dissociatives in higher doses.
[snip]
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sekio
Bluelight Crew
Dissociation from DXM needs pretty high does to be administered... increasing conversion to DXO does increase potency as a dissociative.
The effects of DXM as a dissociative/euphoriant are actually very well-documented, I'm surprised that you haven't come across more reports? Given the easy accessibility of cough syrup (or other DXM preparations) to misguided and/or bored youths via purchasing, theft, or otherwise, there are a plethora of reports out there at every possible dosage level from zero to way too much.
Limpet_Chicken
Bluelighter
Oops,guess from that edit I must have been gouching out and done exactly that. I hate it when I'm typing on (especially laptop) keyboards and either nod off to produce the 'catwalk effect' (when a animal being a member of the order Felidae kept in a domesticated context decides to be a naughty little beggar and daintily pad about on your keyboard)
Or for some reason, opioids often seem to cause slight myoclonus (why is this? other people get this?)
Twitching fingers, fingertips and feet, ankles, wrist mostly, and it often causes me to, whilst not nodding, but fairly well developed influence of the MOR agonist, to repeatedly press a key, have to remove the character then redo both, often several times.
Other than memantine and rimantadine, amantadine anyone know of otherl, similarly low-trapping antagonists? is there a profile available for common NMDA antagonists used either recreationally, medically, in research or a combination of these settings, of their channel residence times? to get some idea and compare side by side rather than have to dig through all the lit manually and dissect each paper bit by bit until finding something relevant, then table it all up?
Memantine, cotcha, if I understand things right, has some similarities to magnesium, in that it gets booted out on glutamate binding quite easily, being a low trapping, low-medium affinity uncomepetitive antagonist, binds harder than magnesium but not massively so, so it can leave the normal function of glutamatergic synaptic activity umolested, whilst blocking excessive calcium currents that would otherwies cause excitotoxicity. As being an uncompetitive antagonist it needs activation by glutamate/aspartate to bind the orthosteric site before memantine can uncompetitively bind its allosteric site on the NMDAr. So, blocking Ca++current production in excess more than it produces blockade of regular, NMDAr-dependent LTP.
Are there any voltage-dependent high-trapping uncompetitive or noncompetitive antagonists available for NMDARs?
I used dxm for a few years everyday. To the best of my knowledge this is extremely accurate to your question.
JohnBoy2000
Bluelighter
Cotcha Yankinov
Bluelight Crew
It reminds me of eslicarbazepine in the sense that it has some specificity for channels that are being often used, therefore mostly addressing the epileptic type neuronal firing and trying to leave alone normal transmission. Although I think it's thought that memantine mostly affects the extrasynaptic NMDAr's and doesn't have too much effect on synaptic NMDAr's.
I took 240 mg to 480 mg overday for like half a decade with benadyrl and inhalational anestheticswith a enzyme inhibitor so its stronger . I would exercise every day for two or so hours on it to prevent prople from notticing. I would practice rapping for speach, walking up and down fast slow eyes open closed one open etc rapidly o n a treadmil and weight train
Prescottdave
Bluelighter
And look how much good it did him. In all honesty I believe daily dosing of over 75 mg has a number of detrimental effects. This may be off topic to NPD but I have a family member that takes DXM 20 mg 2x/day combined with quinidine for Alzheimer's disease. It cost over 500 dollars a month though I imagine part of that is covered by insurance.
Cotcha Yankinov
Bluelight Crew
I suspect daily chronic use of ketamine is not a good thing either but used sporadically therapeutically it can probably be effective for MDD. Same with daily use of ibogaine for opoid use disorder vs. sporadic use.
Daily DXM has been used by some to treat their depression but really the main issue is the psychosis with chronic higher dose use. I think a couple lower doses (100-200mg) wouldn't be too bad, but if the benefit isn't retained off of dosing low or with dosing higher 2-3 times a week then I'd say it's questionable.