ibogaine as a tryptamine

[bravedog]

Ibogaine is a long-lasting tryptamine with interesting traditional and anti-addiction uses. I've read quite a bit about it and am struck by how differently it is described than other tryptamines. In fact before reading TIKHAL I thought of it as a separate class of hallucinogen and was surprised then to learn it is a tryptamine.

I am curious as to how far these differences in description actually derive from the way it is used [set and setting] and how much of its uniqueness is intrinsic. I would be most interested to hear from anyone who has used ibogaine who has also used other psychedelics. I understand that the ibogaine experience as currently structured tends to focus on internal imagery of one's important life experiences - but other psychedelics can also have this effect, especially in a therapeutic context. Does ibogaine identifiably have the characteristics of other tryptamines, such as visual patterns, motion of surfaces, deepening of color, visual tracers, sense that the "doors of perception have been cleansed", etc? Or is it in your opinion intrinsically qualitatively different from other tryptamines? Thanks

bravedog

Reputation Comments on this post:

Top-notch question.

[bravedog]

For what it's worth I just at Burning Man asked Daniel Pinchbeck who has experience w various classic psychedelics and also with ibogaine, whether his experience is that ibogaine is a true psychedelic ie with visual patterns etc like other psychedelic tryptamines and he affirmed it is.

His description of the experience in Breaking Open the Head however like most experience reports of it is focussed on life reflection. I still wonder how much this is an effect of set and setting and how much an intrinsic effect of ibogaine. I remain interested in what others think.

bravedog

[Felonious Skunk]

You've made some interesting points. Although ibogaine has a tryptamine backbone, it is like LSD in that there is so much more to the molecule that one has to wonder how much that backbone really "contributes."

Both of these molecules seem to have effects unique unto themselves.

SWIM is planning on 100mg insufflated experiments in the not-to-distant future.

[chemlove]

SWIM is very interested not in using ibogaine, but he is very interested in reading more about its use especially in Africa!

He also wanted to know if it is used in S. America and if there is any good references as to where i can read more about the experiences (minus erowid)

I have always been interested in the use of Such Tryps like Dmt in other countries and in shamanic activities.

[bravedog]

Originally Posted by chemlove

SWIM is very interested in reading more about its use especially in Africa!
.

Do a google search on Bwiti, the cult which uses it in Cameroon and Gabon. I don't believe it is traditionally used elsewhere.

Mr Skunk, I'd be interested to hear when SWIM tries that 100mg. However I think the strongest traditional experiences are with much higher doses, to over a gram. Also, there are deaths associated both with ibogaine, and also with insufflation of psychedelics not usually dangerous, so please advise SWIM to proceed very cautiously.

bravedog

[Felonious Skunk]

^^^^ You are quite correct, but there have also been some intriguing reports of low-dose benefits. SWIM will probably explore both routes over time.

He's read up quite extensively on the subject, and I'm sure he'll appreciate your good wishes and will pass some back to you, too!

[eltimmy]

NMDA antagonist (in the vein of dextromethorphan and PCP):

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Ann N Y Acad Sci. 1998 May 30;844:245-51.
Effect of ibogaine on the various sites of the NMDA receptor complex and sigma binding sites in rat brain.
Itzhak Y, Ali SF.

Department of Biochemistry and Molecular Biology (R-629), University of Miami School of Medicine, Florida 33101, USA. yitzhak@mednet.med.maimi.edu

Although the alkaloid ibogaine is a potent hallucinogenic agent some indications suggest that it may be useful for the treatment of opioid and cocaine addiction. The neurochemical mechanism(s) underlying ibogaine effects remain unclear. In the present study we investigated the interaction of ibogaine with the phencyclidine (PCP) site located in the ionophore of the N-methyl-D-aspartate (NMDA) receptor complex, with the NMDA receptor binding site, and with sigma binding sites. In well-washed membrane preparations of rat cortex and cerebellum, the PCP sites were labeled with [3H]MK-801 or [3H]1-[1(2-theinyl)-cyclohexyl]-piperidine ([3H]TCP), and the NMDA receptor with [3H]-CGP 39653. The sigma-1 and sigma-2 binding site in rat cortex and cerebellum were labeled with [3H]pentazocine and [3H]1,3-di-o-tolyl-guanidine ([3H]DTG), respectively. Results indicated that ibogaine interacts with high- and low-affinity PCP binding sites in the cortex: Ki(H) = 0.01-0.05 microM; Ki(L) = 2-4 microM, and only with low-affinity sites in the cerebellum: Ki = 2-4, microM. In contrast, ibogaine (> 100 microM) had no affinity for [3H]-CGP 39653 binding sites (cortex and cerebellum). The affinity of ibogaine for sigma-1 and -2 binding sites in cortex and cerebellum ranged from 1.5-3 microM. Since NMDA receptor antagonists (e.g., MK-801) are thought to attenuate opioid withdrawal symptoms and cocaine sensitization, it is possible that binding of ibogaine to the PCP sites contributes to its potential 'endabuse' properties. In turn, ibogaine interaction with sigma binding sites may be associated with its adverse effects.


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NMDA antagonist properties of the putative antiaddictive drug, ibogaine.
Popik P, Layer RT, Fossom LH, Benveniste M, Geter-Douglass B, Witkin JM, Skolnick P.

Laboratory of Neuroscience, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland, USA.

Both anecdotal reports in humans and preclinical studies indicate that ibogaine interrupts addiction to a variety of abused substances including alcohol, opiates, nicotine and stimulants. Based on the similarity of these therapeutic claims to recent preclinical studies demonstrating that N-methyl-D-aspartate (NMDA) antagonists attenuate addiction-related phenomena, we examined the NMDA antagonist properties of ibogaine. Pharmacologically relevant concentrations of ibogaine produce a voltage-dependent block of NMDA receptors in hippocampal cultures (Ki, 2.3 microM at -60 mV). Consistent with this observation, ibogaine competitively inhibits [3H]1-[1-(2-thienyl)-cyclohexyl]piperidine binding to rat forebrain homogenates (Ki, 1.5 microM) and blocks glutamate-induced cell death in neuronal cultures (IC50, 4.5 microM). Moreover, at doses previously reported to interfere with drug-seeking behaviors, ibogaine substitutes as a discriminative stimulus (ED50, 64.9 mg/kg) in mice trained to discriminate the prototypic voltage-dependent NMDA antagonist, dizocilpine (0.17 mg/kg), from saline. Consistent with previous reports, ibogaine reduced naloxone-precipitated jumping in morphine-dependent mice (ED50, 72 mg/kg). Although pretreatment with glycine did not affect naloxone-precipitated jumping in morphine-dependent mice, it abolished the ability of ibogaine to block naloxone-precipitated jumping. Taken together, these findings link the NMDA antagonist actions of ibogaine to a putative "antiaddictive" property of this alkaloid, its ability to reduce the expression of morphine dependence.

PMID: 7473163 [PubMed - indexed for MEDLINE]

[eltimmy]

Kappa opioid agonist (in the vein of salvinorin A):

High affinity ibogaine binding to a mu opioid agonist site.
Codd EE.

R. W. Johnson Pharmaceutical Research Institute, Spring House, PA 19477-0776, USA.

The naturally occurring indole alkaloid ibogaine is of interest because of its reported ability to block drug seeking behavior for extended periods. The compound also potentiates morphine-induced analgesia in mice and reduces certain naltrexone-precipitated withdrawal signs in morphine-dependent rats. Although these results might suggest ibogaine interaction with opioid receptors, previous receptor binding studies (Brain Res. 571:242-247, 1980) found that ibogaine had a Ki value of only 2 microM for the kappa opioid receptor and was virtually inactive in blocking mu and delta receptor binding (Ki > 100 microM). The present investigation of ibogaine interaction with the mu opioid receptor from mouse forebrain labeled with [3H]-naloxone, however, yielded significantly more potent mu opioid Ki values. LIGAND analysis indicated that the data were best fit by a two site binding model, with Ki values of about 130 nM and 4 microM, reflecting ibogaine recognition of different agonist affinity states of the receptor. Inclusion of 100 mM NaCl in the assay to induce the agonist low affinity state of the receptor, reduced ibogaine's inhibition of [3H]-naloxone binding. These results suggest that ibogaine is an agonist at the mu opioid receptor with a Ki value of about 130 nM, potentially explaining ibogaine's antinociceptive effects as well as its reported reduction of opioid withdrawal symptoms and attenuation of drug seeking behavior.

PMID: 7475926 [PubMed - indexed for MEDLINE]

[eltimmy]

>is that ibogaine is a true psychedelic

I wasn't aware that trippy visuals define what a "true" psychedelic is, as if that means much.

[bravedog]

Originally Posted by eltimmy

salvinorin-a, dextromethorphan. PCP, NMDA

But do other psychedelic tryptamines also have any effects on these [dissociative?] receptors?

Does ibogaine have dissociative properties? The experience reports seem just the opposite. But, it would help explain a difference from other tryptamines.

bravedog

[bravedog]

Originally Posted by eltimmy

I wasn't aware that trippy visuals define what a "true" psychedelic is.

Trippy visuals are not at the heart of the psychedelic experience, but they are a good symptom.