-
N&PD Moderators: Skorpio
Monoaminergic Dissociative Anesthetics for depression.
- Thread starter X11400
- Start date
sekio
Bluelight Crew
I would say that they are worth a try for sure.
PCP is probably the better choice of the two though; DXM is more of a SNRI with a dissociative side effect.
Correct dosing is crucial, and is probably on the lower side... yeah, I wasn't depressed when on 150mg PCP but also was arguably barely functional as a human.
You used 150 mg of pcp?
3 were mentioned.
Wow
sekio
Bluelight Crew
I had a stint where I was, in retrospect, totally off the hinges with PCP, yes. Before that I used 3-MeO-PCP as well. I think the highest I pushed it was 200mg or so? My father dragged me to the hospital and got to have a 24 hour psych hold because I was so fried I could hardly form a coherent sentence. Heavy slurring of speech, inability to articulate well, strange gait, whole 9 yards. (And no, I wasn't physically violent or any of that, just... altered.) At least the effects reverse given time. Was only an overnight stay, they decided I was sober by next morning and told me to fuck off.
Higher doses of PCP and its friends (I'd say anything over maybe 50mg) is... unique, for sure. It's absolutely not for everyone and is the kind of thing that a sitter should be involved with, but I have had my share of amazing transcendence as well as a few more negative ones, and regard it as underrated (to the vehement objections of my father, who insists there is no positive effects to be had in dissociative land...)
You confused yourself and I. You said that DXM isn’t antidepressant due to the fact that it’s an SNRI?
Doesn’t that contradict scientific literature?
sekio
Bluelight Crew
Despite popular belief, my understanding is that SNRI/SSRI drugs are less than ideal antidepressant agents, and also have less than ideal side effect profiles. In comparison, I would suggest more NMDA-selective agents are probably a better therapy.
what?
Show me the science and mathematics behind your assertion.
dopamimetic
Bluelighter
Based on experience, I agree with that transporter blockers don't make good options in the long run. DRIs are less problematic, to me, than S/NRIs but they are mostly effective short time and things get bad with tolerance. Not sure whether they just should be avoided before the age of 25 or sth as people using stims since early have similar problems with them like I have with SNRI but they are purely sympthomatic and don't solve or change anything. Just recently read that long term AD use is linked to type 2 diabetes too like it is with antipsychotics, they didnt mention which ones so might be particular substances but sounds bad. Also they mess up sex and make you unable to trip semi permanently, not to mention personality changes and horrible withdrawal (nmda antagonists can do these too).
That said DXM is a decent antidepressant as long as you don't overdo it. While it's a strong SNRI, able to induce panic attacks when done above a few hundred mg (what eg venlafaxine doesn't do but gives you migraine) and has a somewhat benign withdrawal in comparison. It's a SNRI, NMDAi, sigmaergic and very weak, likely insignificant (but that's true with tianeptine at 12,5mg too) opioid.
Never did PCP due to scarcity in Europe, 3-MeO didnt work for me but it does so for others. But I tend to see no potential in K either when the papers tell the opposite. Tolerance to dissociatives abolishes their positive long term effects so you will want to use them as sparingly and low dosed as possible. I remember DXM having a 4-day afterglow in early days.
Was that a statistical analysis or your opinion/anecdotal evidence? All targets matter.
dopamimetic
Bluelighter
It's my conclusion after 10+ years of various S/NRIs, 1+ year of plus or only DXM, various third person longer-term obervations and reports etc. There is very little data about real long term use of antidepressants and there it is mostly only about comparing the efficacy and side effects of various agents but not like the short term (12 weeks?) ones against placebo. It took ages for withdrawal to become generally accepted and some still will tell you it is the initial illness arising again and often there is no choice than to continue on a med as few places have actually prescribable 5-htp, manywhere it's free though and anybody could buy it to get through withdrawal (the most effective remedy to my experience, doesn't work for venlafaxine though as that one has supposedly opioid mechanisms, despite being explicitely developed as a non-opioid tramadol derivate but the effects are reversible by opioid antagonists and w/d feels exactly opioid+SNRI).
The one SSRI in which I am still interested is fluvoxamine as it's the only one with significant sigma agonism. Sertraline is often mentioned but it's an antagonist there and had horrible, psychotomimetic experience with it.
Have to say that I do get the antidepressant effect from dissociatives, from many of them especially the ketaminoids (2F/-DCK, MXE) in that somewhat negative emotions and thoughts are kind of blocked, even with heavy tolerance but overshadowed by rebound ... it is maybe not unlike buprenorphine on which I thought fuck is this chemical useless, it does nothing - but noticed in retrospection that it wasn't a classical mood lift but a partial absence of negative triggers and certainly works in a better way than SNRIs which do change personality not necessarily in a good way (I tend to like what loads of serotonin do though, more so on releasers than on reuptake inhibitors, yet it is more of an addictive likening which makes my natural sober emotional landscape feel unbearable. And they can and do worsen certain negative things too. Just look at the statistics and black box suicide warning. Dissociatives are rapid acting antisuicidals.)
dopamimetic
Bluelighter
Interesting paper about the matter: Novel glutamatergic drugs for the treatment of mood disorders
Molecular targets of glutamatergic drugs for mood disorders.
Notes: Sites of action and regulation for glutamate neurotransmission are shown, and drugs that target each specific site/mechanism are indicated. The specific locations depicted here are representative, though ionotropic and metabotropic glutamate receptors may be located on both presynaptic and postsynaptic cells. Numbers indicate the following targets: (1) NMDAR; (2) AMPAR; (3) Group I mGluR; (4) Group II mGluR; (5) Group III mGluR; (6) Glycine site of NMDAR; (7) Na+ Channel; (8) Ca++ Channel; (9) K+ Channel.
Abbreviations: AMPAR, 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl) propanoic acid receptor; EAAT, excitatory amino acid transporter; Gln, glutamine; mGluR, metabotropic glutamate receptor; NMDAR, N-methyl-D-aspartate receptor; MTEP, 3-((2-methyl-4-thiazolyl)ethynyl)pyridine; PHCCC, (−)-N-phenyl-7-(hydroxyimino) cyclopropachromen-1a-carboxamide; EMCMQM, (3-ethyl-2-methyl-quinolin-6-yl)-(4-methoxy-cyclohexyl)-methanone methanesulfonate; Glu, glutamate; ACPC, 1-aminocyclo-propanecarboxylic acid.
