Naloxone reverses a DXM trip

[fluxy]

I know its not really a discussion, but i know if i asked the question, people would takes sides as to wether it did or didnt.

Well, on the weekend i took around 2000mg of dxm in pure form and was found by the police acting strangely. (luckily they were nice). I was well tripping in 4th plateau and because they saw i had pin point pupils, they shot me with 2mg of Naloxone. Within seconds i was back to 3rd plateau, and able to tell them what had gone on and what id taken, but due to the short duration of naloxone, i was back into the 4th plateau within the hour where i spent the rest of my night in hospital.

so for the record, Naloxone DOES bring you down from a DXM trip, no matter how high the dose. i guess you could do this yourself by mixing a suboxone tab and shooting it if you find yourself getting into places a bit to full on for your liking on dxm.

fluxy

 

[The Monkey Mantra]

I'm gonna say this one thing before I skip town (town being this thread):

I think tripping too hard on DXM is a really fucking STUPID reason to crush up suboxone and shoot it up. You do realize suboxone has a massively strong opioid effect of its own, right? I mean, JEEEEZus!

 

[moonyham]

cops carry around naloxone and can just shoot you up with it as they will? WTF?

 

[MurphyClox]

I would think that naloxone will bring you down just to a small degree (as you said: just from the 3rd to the 4th plateau). It is highly improbable that naloxone will completely interrupt a DMX-trip... DXM is no opioid and acts mainly via NMDA-receptors, at which naloxone is NOT active in any way.

Ah yeah, and shooting any kind of crushed tablets is downright stupid!

- Murphy

 

[dread]

Furthermore, the naloxone in a suboxone tablet has no effect at all, since the buprenorphine will swiftly displace the naloxone from the receptors due to the vastly higher binding affinity.

 

[JahRed24x]

You know what seems to block drugs even more then naloxone is Bupe (Suboxone). I swear Bupe has the ability to block LSD from working, of course block ALL opiates (with the exception of Tramadol (quasi- which DOES seem to work somewhat on subs), and i know when i first started takin subs I even noticed it blocking some of the effects of ganja as well...

 

[The Monkey Mantra]

^^ That's what we're referring to in *all* the above posts. And dread, I think the OP *could have* implied that he wanted to shoot his binder-filled orange-syrup concoction into his bloodstream because of buprenorphine's partial-agonist nature. It wouldn't NEED naloxone to knock any opioid out of the receptors. Anyway, you're right; the naloxone is useless, and Murphy's on it about not shooting up pills. It's a horrible idea, as I kinda implied in this post.

 

[Hammilton]

That'd probably provide a sweet rush on top of the trip, though Especially with neophyte level tolerances.

Is naloxone a significant sigma agonist or antagonist? I honestly don't know if it's agonism or antagonism that produces psychoactive effects, I suspect agonism. And naloxone would be an antagonist mostly likely. That could explain why it knocks down the experience, since AFAIK, DXM has significant effects there.

 

[The Monkey Mantra]

Naloxone doesn't really bind to sigma receptors, as far as the research goes.

 

[benknotdead]

yeah, this actually does work. dxm binds to more than just NMDA receptors. dxm binds to mu opioid receptors as well, and since naloxone is an inverse agonist to those opiate receptors, most of the effects of dxm do actually stop. if you would take a suboxone, then the buprenorphine in it would replace the dxm in those receptors and bind even tighter (the reason why bupe and narcan are put in a pill together is bc bupe binds to receptors as good as naloxone) and the naloxone would take care of the rest.

just tried doing about 500mg of dxm and shooting up about 2 mg of suboxone and my trip came to a complete stop and instead it was replaced with a real fucking good high. the naloxone got rid of the dxm while the bupe took its place. leaving me with an almost floaty vibe, and a real good feeling, like "i have finally landed, journeys over, lets crack a beer and daze out" feeling. sans hangover, sans insomnia.

after tripping for a few hours shoot up 4mg of suboxone. try it. doing that and lighting a huge stogie after a long journey is about the best thing about doing all this shit.

if you mixed the dxm with other opiates however; DO NOT do it. the naloxone reverses the effects of most opiates entirely. which means if you took norcos or some shit during your dxm trip the naloxone would completely fuck you up and give you the reverse effect of taking an opiate. since dxm isnt actually an opiate, the naloxone has a different effect if its just dxm in your system,

 

[adder]

Dextromethorphan is not a mu agonist to a significant degree. Why naloxone is a partial antidote for DXM overdose may be an indirect downstream effect. Also, telling people to try shooting up buprenorphine on top of a high dose of DXM is plain irresponsible. Both are CNS depressants and both depress breathing, such a combination may easily turn out fatal. I took a low dose of DXM (150mg) on top of 4mg of Suboxone on a few occasions and both my heart-rate and breathing were severely slowed down. Don't do this.

 

[sigmond]

Somewhat off topic but is there a drug that could help stop someone who was having a 'bad trip'?

To be specific, stop the effects of lsd or other hallucinogens the same way naloxone works in regards to an opioid overdose.

(apologize if this has been answered already, If so I missed it)

Thanks

 

[yaesutom]

You know what seems to block drugs even more then naloxone is Bupe (Suboxone). I swear Bupe has the ability to block LSD from working, of course block ALL opiates (with the exception of Tramadol (quasi- which DOES seem to work somewhat on subs), and i know when i first started takin subs I even noticed it blocking some of the effects of ganja as well...

I have also noticed this - suboxone blocking 4-aco-dmt (what was left of the mild trip, was a more psychotic trip) and also methallylescaline. Posted about it and people said they haven't noticed this. I noticed.. not knowing why (still don't know why it would dampen a trip, its not supposed to be a serotonin receptor antagonist).

Weird things happen sometimes leading me to think some of these drugs have effects we don't know about (or even weird downstream effects).

Somewhat off topic but is their a drug that could help stop someone who was having a 'bad trip'?

To be specific, stop the effects of lsd or other hallucinogens the same way naloxone works in regards to an opioid overdose.

I've used Remeron (mirtazapine) to completely block 2c-t-4, 7, and DOC trips. The trip effects just stop about 45 mins after eating 15mg.

 

[adder]

I suppose it has something to do with kappa antagonism. Kappa inhibition may block downstream effects of 5-HT2A activation. When a ligand activates its target receptor, it doesn't end there, there's a downstream of effects that follow. My hypothesis is that both 5-HT2A agonist psychedelics and dissociatives (both kappa agonists and NMDA antagonists/sigma agonists(?)) may cause similar downstream effects to some extent. However, I'm far from having enough knowledge and resources to look deeper into it.

 

[sigmond]

I've used Remeron (mirtazapine) to completely block 2c-t-4, 7, and DOC trips. The trip effects just stop about 45 mins after eating 15mg.

This is interesting...

(preface: my knowledge of drug activity in the brain is limited)

I have no idea if this is even possible.

I was thinking if you could create a blocker similar to naloxone for MDMA or LSD it might help with the re-scheduling efforts going on.

If some day these drugs do get approved for clinical use people are going to report bad experiences which I fear could put these drugs back to where they are now.

Did I stump sekio? If so, I want a special a title under my name.

 

[adder]

Mirtazapine and a related drug Mianserin are 5-HT2A antagonists among other activities.

 

[IndustrialStrength]

^ Interesting. Sorry if a bit off topic to the thread but pertinent to BL as a whole.

Someone should update the BL Wiki on that then.
As Anti-Depressants & Recreational Drugs in the BL Wiki states...

Hallucinogens

Hallucinogens seem to be MUCH stronger in combination with Mirtazapine, so please be VERY CAREFUL! A dangerous interaction with shrooms has been observed in one person taking Mirtazapine. Please avoid hallucinogens while taking mirtazapine or dose very carefully.

Going off Adders post I would have been quite disappointed had I chosen to use a hallucinogen.
Though I don't usually use that class of drugs in general but I digress.
Do you think that Mirtazapine would interact with Ketamine being a dissociative as opposed to a hallucinogen?
As from your statement I don't know if I can trust the Wiki on that either.

As so far I've found Wikipedia has more accurate information regarding Mirtazapine than BL.
Which IMHO is a sad state of affairs.

Such as the statement on Wikipedia

With its newly understood properties of 5-HT2C inverse agonism, it is being investigated and shown to lower drug seeking behaviour, conditioned place preference and the rewarding effects of substances such as methamphetamine in various human and animal studies.

References for above statement.

NSFW:

73. Graves, SM; Napier, TC (2012). "SB 206553, a putative 5-HT2C inverse agonist, attenuates methamphetamine-seeking in rats". BMC Neurosci 13: 65. doi:10.1186/1471-2202-13-65. PMC 3441362. PMID 22697313.

91. Colfax, GN; Santos, GM; Das, M; Santos, DM; Matheson, T; Gasper, J; Shoptaw, S; Vittinghoff, E (November 2011). "Mirtazapine to reduce methamphetamine use: a randomized controlled trial". Arch. Gen. Psychiatry 68 (11): 1168–75. doi:10.1001/archgenpsychiatry.2011.124. PMC 3437988. PMID 22065532.

92. Herrold, AA; Shen, F; Graham, MP; Harper, LK; Specio, SE; Tedford, CE; Napier, TC (January 2009). "Mirtazapine treatment after conditioning with methamphetamine alters subsequent expression of place preference". Drug Alcohol Depend 99 (1–3): 231–9. doi:10.1016/j.drugalcdep.2008.08.005. PMID 18945553.

Since the following is pertinent mostly to myself I will NSFW it; it applies to the above.
It is the main reason I posted the above statement as anecdotal evidence, my own, supports it.
I appreciate those that choose to read & answer it.

NSFW:

From my own anecdotal evidence Mirtazapine seems to dampen the "rush" from opiates.
As though I haven't used IV for years until a few 1 offs recently it seemed that I didn't get the effect I expected.
As I've been on a taper (not by choice) taking 135mg ER Morphine for approx. 2 months now & thought my tolerance should have dropped to a point that 8mg IV Dilaudid should have had a rush.
I did get a nice feeling of warmth & a bit of a come up into a high.
I also caught a nod though I still was experiencing carry over effects from the prior days usage of Phenibut.
Which made me wonder doubly as to the lack of a rush...
As IV Dilaudid from past experience & from the general consensus usually carries a good rush.

Note that I was in withdrawals at the time as I usually don't get a rush from opiates if I'm not.
Also keep in mind that I've had a massive tolerance in the past which seems to be permanent.
IE. At one point I'd wear 2 100mcg/hr Fentanyl Patches at a time;
& shoot 50mg Oxymorphone on top for mediocre high.

Also even though it's been 2 months I've not adjusted to the 135mg ER Morphine dosage.
As I'm still sick every day, prior dosage was 60mg ER Morphine x3 Daily & Dilaudid 8mg x6 Daily.
Though I didn't always use all the Dilaudid. Though what I did use was usually nasally.
As I hadn't used IV in years till as of late as I couldn't handle the dual w/d's of Opiates & Benzo's both.
After a few months I had to get a break as like I said haven't adjusted, though am trying to substitute Phenibut;
for the Klonopin 6mg that I'm currently tapering far to rapidly; at 3mg ATM.
But I digress the Benzodiazapines & Phenibut are irrelevant to the main question regarding Mirtazapine.

Which is do you think that Mirtazapine could be blunting the "rush" or that it might just be from my;
"permanent" tolerance, as I don't have many left & haven't had the chance to try doing a higher dosage.
The "permanent" tolerance statement comes from my lack of adjustment & lack of a rush.
Though now I'm questioning the lack of rush as possibly being Mirtazapine related.
Also while I'm asking questions regarding that Ketamine question; I've only ever done it a few times nasally.
I only have a small amount left & was planning on trying it IV, do you think the Mirtazpine would affect it?
For reference I'm on 15mg Remeron daily.

Also while I'm asking questions for those with experience does the K hit;to quickly to notice an opiate "rush"?
As I planned on mixing it with Dilaudid to avoid being in withdrawals & ruining the Ketamine experience.
However, if you get the Opiate rush along with the Ketamine effects I planned on using a high enough dosage to get a decent "rush" if it was possible to do so while on Mirtazapine.

Thanks to anyone who takes the time to read & answer these questions.
I apologize if they are off topic to the thread but are seemed to relate to Adders response.
As such I felt they were appropriate to ask as long as NSFW'd.
If this is not the case let me know & I will delete this post & PM directly or find another way to answer the question.

 

[adder]

I have no idea by what mechanism mirtazapine could make serotonergic psychedelics stronger or even "true" anticholinergic hallucinogens because it doesn't have much anticholinergic properties itself either. Like I wrote, both mianserin and mirtazapine are 5-HT2A antagonists, however, mianserin is certainly much more potent than mirtazapine at equivalent therapeutic doses. I think we may trust Wikipedia on the values here as they come from a proper source.

What's also interesting though is that mianserin and mirtazapine are also kappa partial agonists, again mianserin is much stronger than mirtazapine but it's pretty weak anyway. I actually experienced fairly simple CEVs after combining 30mg of mianserin with my daily Suboxone dose, it was a weird experience, however, I don't know if it may be attributed to its effect on kappa opioid receptors as buprenorphine is a much more potent kappa antagonist. But then again I doubt it could potentate psychedelics through partial kappa agonism if it's a much more potent 5-HT2A antagonist with an affinity higher than most of popular psychedelics except NBOMe's, lysergamides, and some DOx amphetamines.

 

[serotonin2A]

I suppose it has something to do with kappa antagonism. Kappa inhibition may block downstream effects of 5-HT2A activation. When a ligand activates its target receptor, it doesn't end there, there's a downstream of effects that follow. My hypothesis is that both 5-HT2A agonist psychedelics and dissociatives (both kappa agonists and NMDA antagonists/sigma agonists(?)) may cause similar downstream effects to some extent. However, I'm far from having enough knowledge and resources to look deeper into it.

It is pretty well known that mu-agonists suppress the effects of 5-HT2A activation. The kappa receptor doesn't appear to play a role because the interaction doesn't occur with kappa-selective ligands.

http://www.ncbi.nlm.nih.gov/pubmed/9881863

http://www.ncbi.nlm.nih.gov/pubmed/12909198

http://www.ncbi.nlm.nih.gov/pubmed/17535909

http://www.ncbi.nlm.nih.gov/pubmed/17102981

 

[atara]

I was well tripping in 4th plateau and because they saw i had pin point pupils, they shot me with 2mg of Naloxone. Within seconds i was back to 3rd plateau, and able to tell them what had gone on and what id taken, but due to the short duration of naloxone, i was back into the 4th plateau within the hour where i spent the rest of my night in hospital.

Hm, it sounds like DXM has opioid effects which are countered by naloxone, but that doesn't mean the other effects are. Dissociatives, including DXM, generally make your pupils larger, not smaller, but since DXM has some µOR affinity it's possible that at higher doses the opioid effects predominate -- DXM's µOR affinity is roughly half of DXO's NMDA affinity. Since there seems to be agreement on a division between 3rd and 4th "plateau" experiences, and naloxone took you from 4th to 3rd, I suggest that the 4th plateau is when the opioid effects of DXM start to shine through the dissociation, which explains your pupils and your reaction.

But buprenorphine and naloxone have something else in common, too: they are both kappa-opioid antagonists (bupe is actually more potent), which as adder mentioned, could be antipsychotic on its own.

It is pretty well known that mu-agonists suppress the effects of 5-HT2A activation. The kappa receptor doesn't appear to play a role because the interaction doesn't occur with kappa-selective ligands.

DXM has no 5-ht2a affinity, so who cares?

I have no idea by what mechanism mirtazapine could make serotonergic psychedelics stronger or even "true" anticholinergic hallucinogens because it doesn't have much anticholinergic properties itself either.

Mirtazapine is a potent alpha-2 adrenoreceptor antagonist. These are known to enhance the formation of Olney's lesions in rats dosed with NMDA antagonists (eep!!) so it's possible that this also enhances the primary effects of dissociatives. However this combination is sort of obviously a bad idea, because even though we're still not sure if Olney's lesions form in humans it isn't wise to push your luck.

Also, I should probably make a note somewhere that this combination is contraindicated.