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Benzomorphans arn't too weak

Black said:
is there more than one kind of kappa receptor?
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AFAIK no, just mu, kappa, delta.

lysergication said:
Also, when researchers speak about dysphoria mediated by the KOR agonism, are they speaking about this weirdness or it's pure dysphoria (opposite to euphoria) and if it is, why don't we experience this dysphoria with salvinorin a ?
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Good point indeed! I enjoy Salvia a lot albeit it's not the easiest to take. But the "weirdness" that you mentioned is exactly the stuff I like...no dysphoria at all to me. Or only after higher doses (like after a Salvia blackout)?
 
Yes kappa agonists can counteract (somewhat) the mu receptor, and this may prove unenjoyable to most (highly selective κ-agonist like salvinorin).
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post 24

This seem to be the "dysphoria" researchers talk about, a counteraction at the MOR...wich is not per se enjoyable for the vast majority of people but not that dysphoric. Simply, most people don't want to repeat the experience because it's not euphoric, so "what's the point to do so" ?
 
AFAIK no, just mu, kappa, delta.
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There's at least two mu subtypes, appropriately named 1 and 2. one for classic euphoria, two for sedation and respiratory depression (think propoxyphene).

Oh, and while I do enjoy the effects of Salvia for an occasional intense trip, pentazocine is far to freaking weird.

I think it's FnB who talks about getting lost in your own bathroom. Salvia is too brief for that to be problematic- pentazocine could turn being lost into an afternoon adventure.
 
I think it's FnB who talks about getting lost in your own bathroom. Salvia is too brief for that to be problematic- pentazocine could turn being lost into an afternoon adventure
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if we want to be precise, it's the (-)-pentazocine that would do this precisely because of the KOR agonism ?

So, (-)-pentazocine is not enjoyable because of the long duration ? You'd be in a salvia space (or KOR agonist space) for way too long, that would be the problem ? what about the metazocine then (if I understand correctly, it seems that it's the (+)-metazocine that would be like pcp - paper)?
 
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I believe that metazocine is a sigma ligand, but not a noncompetitive NMDA antagonist. Not sure.

Yeah, because of long duration it makes it impractical as a drug of abuse. short duration kappa agonists aren't really DOA either, though. Salvia isn't a drug of abuse in any real sense of the word. smoked DMT really isn't either, these are better considered sacraments than anything- just because recreational use is impractical, incompatible with the effects.

which isomer is responsible really doesn't matter because the commercial prep people will use isn't stereospecific, unfortunately.
 
Does anyone know off-hand which enantiomers of pentazocine are found in talwin (ratios, or is it equal parts)?

As i mentioned in another post, and as someone touched on, the kappa agonists may not cause dysphoria per say, but they appear definately less euphoric than pure mu agonists. I've had alot of experience with high doses of IM/IV butorphanol (also a kappa agonist), which is an exceedingly strange drug. It had a strange tendency to make my vision very dim, in that everything appeared as though i was looking through extremely heavy sunglasses (similar to those you wear after seeing an optometrist), at times loosing sense of color completely, with everything appearing as a deeply faded sepia. It can be uncomfortably psychedelic in high doses, but again, strictly speaking, not dysphoric, just highly unusual. The pyschedelic properties from high doses are somewhat unlike salvinorin, however the darkening or even sepia vision (and to a lesser extent, auditory hallucinations) appears to be a common featue in both these drugs. I recall one time after taking 16mg IM i walked down to the market, and as i was shopping everything got extremely dim, i could no longer read the labels (vision was not fuzzy though, just so dark). Walking home took a very long time, as it was night, so it was already quite hard to see.

In regards to butorphanol, highest doses i ever experimented were 30mg IM, and 20-22mg IV; these were both unpleasant, the IV being significantly less unpleasant. The 30mg IM resulted in physical pain, a tearing or splitting in half sensation that i have gotten from salvia (reminds me of Mohammed in Dante's Inferno)...
 
negrogesic said:
however the darkening or even sepia vision (and to a lesser extent, auditory hallucinations) appears to be a common featue in both these drugs.
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At least to the extend of Salvinorin: Yep! Definitively!
 
Some pure kappa-agonists (enadoline for example) have been tested in small clinical trials, and they all lead to severe dysphoria and psychosis. Kappa opioids aren't the way to go in my opinion. Better try some delta agonist.
 
Yes delta agonists do cause convulsions, but the convulsant dose is quite far above the dose for onset of effects, and I'm not sure they would be that much worse than say tramadol. Also some delta agonists have been developed that don't cause convulsions, so it may not be a class effect.

All this talk about kappa agonists makes me want to try pentazocine and butorphanol now! Even though no-one really seems to enjoy them that much...
 
butorphanol absolutely blows.

Pentazocine is interesting in some ways, but weird as hell.

I had butorphanol for my dog post-neuterization and, unlike just about every opiate in the world, it caused massive diarrhea.
 
Generally speaking, none of these drugs are particularly desirable, personally I felt butorphanol was better (and more sedating) than pentazocine (both being better than nalbuphine), however I imagine this could vary significantly by individual (i forgot whether it was pentazocine or nalbuphine than was more effective in women with red hair) . When i experimented with levorphanol a couple years later, i did have what appeared to be butorphanol flashbacks (obviously levorphanol and butorphanol is an unfair comparison, im not insinuating that levorphanol is significantly similar, but there are a few parallels).

Ham-milton: had you been using opioids prior to taking butorphanol, or were you perhaps already opioid dependent? Even at huge doses i never became sick in that sense, but i had no tolerance to other opioids at the time. I'm not sure what route you used, but IV was far more pleasant and less disturbing than IM (i found this to be true with IV ketamine versus IM, it was far more recreational). All this aside, the drug does have a particularly "dirty" feeling to it...
 
nalbuphine, I think. Or maybe butorphanol.

it was one of those two oddities, I think the former.
 
Ham-milton: had you been using opioids prior to taking butorphanol, or were you perhaps already opioid dependent? Even at huge doses i never became sick in that sense, but i had no tolerance to other opioids at the time. I'm not sure what route you used, but IV was far more pleasant and less disturbing than IM (i found this to be true with IV ketamine versus IM, it was far more recreational). All this aside, the drug does have a particularly "dirty" feeling to it...
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I was opiate dependent, but I waited a full 60+ hours (after I had taken the last of my moms generously gifted 10/250(or whatever the lower APAP content level is) hydrocodones.

I only experienced mild diarrhea, nothing bad. The dog was the one with horrible disgusting diarrhea.
 
Isn't it the case that there are kappa receptors spread throughout the brain in different areas and activation of ones in certain areas cause certain effects while activation of others causes different effects?
 
I'm sure that's true to a degree, but I don't see how a kappa agonist could activate only receptors in certain parts of the brain; it should have affinity to all the kappa receptors it comes across, and since they'll diffuse throughout the blood, it seems like they should come across any kappa receptor in any part of the brain equally likely.

I'm not sure, though.
 
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