Hallucinogens - What's in a Name? or Defending the Indefensible

From Maps Bulletin XIII number 1, article by Gary L. Bravo and Charles S. Grob
Short and smart...
Archived here, PDf here
Reproduced here for educational purposes
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Dr. Lenderts raises important and thought-provoking points in the ongoing dialogue over the proper nomenclature for these plants and chemicals which are the subject of scientific inquiry in the pharmacological, medical, psychological, anthropological and sociological literatures. We have no issue with his thesis that the term "hallucinogen" is in some ways reductionistic and misleading as to the myriad and profound effects these substances may potentially manifest in the brains, minds and souls of users. However, the issue as we see it is to identify a useful terminology which can be agreed upon by all who care to communicate about these protean substances and be recognized by those receiving these communications.

The term "hallucinogens," whether rightly or wrongly, and much to the chagrin of many who would prefer terms such as "entheogens," "psychedelics," or "visionary plants and drugs," has become the accepted nomenclature in the scientific and anthropological literature. For example, an Internet search of the biomedical literature using the words "entheogenic," or even "psychedelic," would probably not generate the desired results for the inquirer, whereas the term "hallucinogenic" most likely would.

In their classic text Plants Of The Gods: Their Sacred, Healing and Hallucinogenic Powers, Richard Evans Schultes and Albert Hofmann do not equivocate in their use of what they consider to be the appropriate term. Over the last hundred years various investigators have alternatively proposed a bewildering nomenclature, including, though not limited to, "deliriants," "delusionegens," "eidetics," "entheogens," "misperceptinogens," "mysticomimetics," "phanerothymes," "phantasticants," "psychedelics," "psychodysleptics," "psychogens," "psychointegrators," "psycho-somimetics," "psychotaraxics," "psychoticants," "psychotogens," "psychotomimetics," and "schizogens." Each of these terms has its particular advantages, yet all fall short of encompassing the entire range of reactions these substances are known to induce.

Acknowledging that no individual appelation is entirely acceptable, it may be instructive to explore the etymological root of the contested term "hallucinogen." As clarified by Ralph Metzner, prolific writer, scholar and early explorer of altered states phenomenology, the Latin root of "hallucinogen" is hallucinari, or elucinari, which translates as "mind wandering" or "mind traveling." By moving beyond the obvious association to hallucination, which itself is defined as a false perception or false idea, and examining "hallucinogen" from the perspective of the induction of mind voyaging, the term is no longer constrained within the fixed, pathological framework Dr. Lenderts suggests.

There are many words in the English language which no longer are referent to their original meaning. We would wish that by using another term for "hallucinogenic" or "psychedelic" or "entheogenic" plants and chemicals -- if we could all agree on one -- that we will challenge or even change the preconceived notions and prejudices of others, but we're not necessarily convinced that this would be the case.

Our argument is basically a practical one -- the key is context. Pioneer pharmacological researcher Sasha Shulgin once told us, when asked about the debate between usage of the term "entheogen" versus "psychedelic," that if you talk to most people "on the street" and refer to entheogens, they won't know what you're talking about, but if you refer to psychedelic drugs, they probably would.

Most likely there will be no resolution to the dilemma of what to call these substances, and they will continue to harbor differing labels depending on the set and setting of the speaker. The term "entheogen" may even become the accepted referent in the religious and spiritual literature. But in the meantime, can't we all just get along?

Current theory on hallucinogen : small population of rhythmic neurons getting hyper-excited by special activation of 5HT2A receptors by psychedelics

Bill Connelly in the maps forum provides a very nice review of recent work on hallucinogens :

There's been a lot of (well deserved) coverage of the recent renaissance in the clinical study of hallucinogens, but quietly, the physiological/pharmacological study of hallucinogens, has also been advancing.

(When I say hallucinogens, I mean, in this context, LSD/mescaline like compounds, i.e. chemicals which activate the subclass of serotonin receptors known as 5-HT2A receptors).

Three papers spring to mind, published in the some of the most influential science journals, including Science, and the Proceedings of the National Academy of Science (PNAS).

It has been known for a long time that hallucinogens increased excitation in the brain, and specifically in the cortex, that is to say, that the connections between neurons (synapses) became more active in the presence of hallucinogens, and the kind of synapses that became active were the type that made neurons more likely to fire action potentials and signal to other neurons. These synapses belong to neurons which are being activated by the hallucinogens, but where to these neurons reside? As brain cells are capable of making connections from one end of the brain to the other, it could be anywhere. The likely hypothesis was a region of the brain called the thalamus. This is the main relay in the brain for most sensory and all motor connections, and on top of that, reciprocal connections between the cortex and the thalamus are believed to underpin consciousness in the round. Modulating signalling through the thalamus could explain the powerful effects hallucinogens have on perception and thought. However, in a paper published in Science, (the best or second best Science journal in the world)a multidisciplinary team, including G. Aghajanian from Yale University,using genetic manipulation of mice, so that they only expressed 5-HT2A receptors in the cortex, and no where else, showed that these mice were received the enhanced excitation caused by stimulating the 5-HT2A receptor; showing that the hallucinogen induced excitation in the cortex by directly activating cortical neurons.

Another paper published in Neuron (the second ranked pure neuroscience journal) revealed several other interesting results. A chemical known as Lisuride activates the 5-HT2A receptor, however in humans, it does not produce hallucinations. This has been paradox in hallucinogen research for some time. This paper revealed that Lisuride, though a 5-HT2A receptor agonist, activates genes in a completely different pattern than 6 hallucinogens studied (DOI, DOM, DOB, LSD, Mescaline and psilocin), and these 6 hallucinogens produced a very similar pattern as each other . Indeed, Lisuride was unable to induce any of the changes in neuronal excitability that LSD could, and was able to block that LSD induced changes. This indicates that Lisuride activates the 5-HT2A receptor, but in a fashion completely different to hallucinogens. Also they showed that selective restoration of 5-HT2A receptor function in the cortex, allowed these mice to show the same hallucinogen-induced behaviours noted in normal mice (head twitch); further indicating that 5-HT2A receptors in the cortex mediated the behavioural manifestations of hallucinogens.

Finally a recent (May 29th) publication in PNAS showed once and for all the source of the hallucinogen-induced excitation. It was demonstrated that the increase in excitation is caused by a small population of neurons which are highly sensitive to hallucinogens. These neurons begin firing constant action potentials in the presence of 5-HT2A receptor agonists. It is these neurons which the must synapse onto a large population of cortical neurons,which these cause the increase in synaptic function recorded previously.

These papers collectively tell us that that likely mechanism of hallucinogens is by causing a small population of cortical neurons to become hyper-excited, which then increases excitation in other neurons. What it does not tell us is what special properties these neurons have that allow them to produce such marked changes in human psychology (or whether they even exist in humans).

Cortical 5-HT2A receptor signaling modulates anxiety-like behaviors in mice.
Weisstaub NV, Zhou M, Lira A, Lambe E, González-Maeso J, Hornung JP, Sibille E, Underwood M, Itohara S, Dauer WT, Ansorge MS, Morelli E, Mann JJ, Toth M, Aghajanian G, Sealfon SC, Hen R, Gingrich JA.
Science. 2006 Jul 28;313(5786):536-40.

Mechanism of the 5-hydroxytryptamine 2A receptor-mediated facilitation of synaptic activity in prefrontal cortex.
Béïque JC, Imad M, Mladenovic L, Gingrich JA, Andrade R.
Proc Natl Acad Sci U S A. 2007 Jun 5;104(23):9870-5.

Gonzalez-Maeso J, Weisstaub NV, Zhou M, Chan P, Ivic L, Ang R, Lira A,
Bradley-Moore M, Ge Y, Zhou Q, Sealfon SC, Gingrich JA.
Hallucinogens recruit specific cortical 5-HT(2A) receptor-mediated signaling
pathways to affect behavior.
Neuron. 2007 Feb 1;53(3):439-52.


--
Bill Connelly
Assistant Research Fellow
Department of Pharmacology
University of Otago

Psychedelics and Synpatic Plasticity

This goes in the direction of my thesis that psychedelics can induce temporary plasticity allowing for a neural remapping, thus allowing to go beyond stuck habits and prejudices.


Adapted from the Maps forum
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One interesting study analyzed LSD effects. It was found was that it stimulated expression in genes related to "synaptic plasticity" - that is, the brain's ability to rewire itself, metaphorically speaking - and genes related to memory consolidation. This suggests that LSD experiences do indeed encourage learning on very powerful and basic levels.

See the article here

Nice 3D string art modeling

http://forum.isratrance.com/viewtopic.php/topic/104751/forum/19

Meditation and Psychedelics