Psychedelic Information Theory : Chapter 12
Neural axons in the human brain are always branching and creating new synaptic connections to facilitate learning and development. Like the toning and bulking of muscle mass, neural connectivity, developmental growth, and plasticity are based partly on genetics and partly on the “use it or lose it” principle; the more you use a neural pathway the more robust and responsive it will become, the less you use a pathway the weaker it will become. Training and repetition build faster and more responsive connections. The more a neuron or assembly of neurons is used in a specific exercise, the faster and more responsive those neurons will become when performing that exercise. This is how the brain learns new things and integrates new skills. Training, repetition, and reinforcement leads to long term changes in synaptic connectivity. These are the basics of neuroplasticity.1
Neuroplasticity is the physical mechanism which makes shamanism and psychedelic therapy viable. In dreaming neuroplasticity is stimulated in response to daily routine and anxiety; in hypnosis neuroplasticity is stimulated in response to suggestion and reinforcement. In shamanism neuroplasticity is stimulated in response to dose, set, and setting. The efficacy of psychedelics in both shamanic transformation and clinical therapy relies on their unique ability to decouple the cortex, disassociate ego structures, and stimulate archetypal identity regression and personal transformation. No other class of drugs can claim to have such a radical effect on personality; radical personality changes in response to brief psychedelic exposure implies neuroplasticity.
While there is no laboratory research to indicate that psychedelics stimulate neuroplasticity, there is evidence that psychedelics can produce long-term changes in personality.2 People who take psychedelics sometimes adopt a new manner of dress, a new spirituality, perhaps even a new name to go with their new identity.3 Self-reinvention is an integral part of psychedelic metaprogramming and subculture. The forging of a new identity does not always happen in a single psychedelic session, but psychedelic experimentation can easily become a catalyst for sudden and radical personality transformation. These basic observations make a case for psychedelics as facilitators of long term identity modification and neuroplasticity.
The Case for Psychedelic Neuroplasticity
Psychedelics can stimulate recall of lost memories and can also generate false memories; lost memory reconsolidation and false memory imprinting implies neuroplasticity. The brain builds tolerance to psychedelics quickly, but psychedelic tolerance can be surpassed by successively ingesting larger doses.4 Successive dosing and increasing levels of tolerance implies stress-based neuroplasticity. In the case of hallucinogen persisting perception disorder (HPPD), the subject retains some of the visual effects of hallucinogens long after the drug should have metabolized;5 persisting reactions to neural stress imply neuroplasticity. Psychedelics have been used to facilitate cult induction and programming;6 indoctrination implies identity-based neuroplasticity. Psychedelics induce peer and mate bonding in tribal subcultures; bonding implies identity-based neuroplasticity. Psychedelics can create positive long-term changes in mood and outlook;2 long term outlook changes imply neuroplasticity. Finally, while lying in darkened silence the psychedelic state resembles a deep dream-like trance; dreaming is known to facilitate memory compression and long-term memory potentiation (LTP).7 Any drug which facilitates extended dream-like states should also facilitate memory compression, LTP, and neuroplasticity.
In programmatic terms the hallucinogenic interrupt can be thought of as a back-door or reboot mechanism that allows the subject to enter a visually driven ego programming and debugging matrix; this state would be similar to hypnosis mixed with an element of lucid dreaming or creative visualization. To stretch the computer metaphor further, in the absence of hypnotic suggestion or shamanic control, the psychedelic debugging matrix will naturally drop into a maintenance mode where anxieties are brought to the fore like a screen-saver programmed to browse through repressed salient forms arising within chaotic patterns.8 All of these programmatic metaphors for psychedelics are accurate, and all imply a spontaneous cataloging, compression, or re-organization of existing synaptic memory via nonlinear eidetic emotional cues; this implies synaptic testing, bonding, and neuroplasticity.
Physiology of Psychedelic Neuroplasticity
Hallucinogens which target the 5-HT2A receptor can influence cellular functioning via the activation of G proteins and secondary messengers. The signaling pathways mediated by the 5-HT2A receptor include the activation of PKC and MAPK, protein kinases which energize enzymes to perform complex cellular maintenance. The activation of PKC undoubtedly plays an active role in the production and maintenance of long term memory. Evidence shows that inhibiting PKC activation in the cortex for as little as a few hours can cause the rapid erasure of long-term memory associations.11 It is obvious that this kinase is a fundamental part of memory formation and retention, and it is not unreasonable to assume that drugs which stimulate PKC activity may enhance or alter the processes of memory formation, recall, retention, and plasticity.
The processes by which PKC mediates memory associations is still unknown, but the primary assumption is that PKC interacts with diglycerides (DAG) at the intracellular membrane to mark energetic signaling areas for receptor formation and synaptic strengthening. The secondary signaling cascade goes like this: The 5-HT2A receptor is stimulated, activating phospholipase C (PLC) in the cell membrane, which then chops a phospholipid (PIP2 or PI) at the membrane into an IP3 group and DAG. The DAG stays near the membrane while IP3 activates the release of Ca2+ from the endoplasmic reticulum, which then activates PKC, which allows PKC to carry energy back to the cell membrane near the DAG site before activating other enzymes and intracellular substrates. PKC performs its job by moving phosphate groups around the cytoplasm and activating cellular enzymes such as adenosine which forms into AMP, ADP, and ATP by carrying phosphate groups in chains of up to three at once, allowing metabolic energy to move to other sites throughout the cell. The addition and removal of phosphates to and from proteins is a fundamental part of all organic metabolic processes; 5-HT2A agonists stimulate this phosphorylation process through PLC, IP3, Ca2+, and subsequent PKC activation.
The fact that 5-HT2A agonists stimulate PKC and fundamental metabolic processes indicates a strong case for psychedelic neuroplasticity. It is interesting to note that Salivinorin A, from Salvia divinorum, also appears to activate these same phosphorylation pathways through the k-Opiod receptor.12 And, of all the hallucinogenic compounds that occur in nature, psilocybin (found in magic mushrooms) is the only one that comes with its own phosphate group, and it also appears to be the weakest tryptamine agonist at the 5-HT2A receptor.13 While it is tempting to assert that PKC phosporylation is at the root of all hallucinogenesis and psychedelic effect, it has been demonstrated that 5-HT2A mediated PI hydrolosis is not always a good indicator of psychedelic potency.14 Although there are multiple factors responsible for hallucinogenesis, psychedelic stimulation of PKC activity undoubtedly plays a role in perturbing and stimulating persistent memory functions and promoting potential potent neuroplasticity.
Other research indicates that LSD activates intracellular mechanisms to promote expression of genes responsible for encoding c-Fos and Arc proteins, particularly in the pre-frontal cortex (PFC).15 c-Fos is essential to cell proliferation, differentiation, and cellular defense, while Arc (activity-regulated cytoskeleton-associated protein) regulates the structure and plasticity of neural cytoskeleton architecture, the very scaffolding which maintains neural shape and stability. By activating expression of c-Fos and Arc proteins in PFC neurons, LSD may promote plasticity, cell proliferation, cell repair, and synaptic generation in neurons responsible for identity. Presumably any selective 5-HT2A agonist will produce similar results, making hallucinogenic tryptamines primary candidates for cellular signal strengthening and identity-based neuroplasticity.
Positive and Negative Plasticity
Shamanic transformation may stimulate neuroplasticity by helping the subject realize a more transcendent or spiritually integrated vision of themselves. The logic follows that transformation of the inner self will then reinforce positive personality traits and drive outer behavioral changes to synchronize with inner idealization. The shamanic transformation is not instantaneous, but instead follows an integrative process of synaptic testing and reinforcement over a period of days to weeks. Some psychedelic therapy stimulates neuroplasticity using techniques similar to the ten-step program employed by Alcoholics Anonymous (AA), where the subject takes a clinical inventory of their life and behaviors and assesses each area where they need forgive, accept, or make changes. In psychedelic therapy the process of uncovering and working through maladaptive pathways is called catharsis; the process of wiring new synaptic pathways and reinforcing new behaviors is called integration. These are examples of positive psychedelic plasticity used to maximize positive social integration. These processes are sometimes slow and require an amount of mental discipline and behavioral follow-through for success.
There are many examples of negative psychedelic neuroplasticity. Renegade schools of ayahuasca sorcery and witchcraft employ some of the most elaborate and lethal mind-games ever devised, including the constant fear of attack by rival sorcerers through poisons, curses, dream invasion, and magical darts that may induce paralysis, cancer, death, or insanity.9 The traditional shaman's constant stress of exposure to the effects of black magic mirrors paranoid psychosis and post-traumatic stress disorder; this implies negative plasticity. Exposing any subject to extended and repeated psychedelic sessions may force stress-driven neuroplasticity associated with PTSD, torture, isolation, and sensory deprivation. Psychedelics may speed techniques of ego deprogramming and imprinting associated with brainwashing or cult-indoctrination;6 this implies mind control and negative neuroplasticity. Psychedelics may aid in imprinting or reinforcing delusional, messianic, paranoid, sociopathic, antisocial and megalomaniacal identity traits;10 this also implies negative neuroplasticity.
Tribal Imprinting and Viral Neuroplasticity
One of the most interesting aspects of psychedelic experimentation is that psychedelics can catalyze spontaneous organization of tribal subcultures and grassroots political movements. According to PIT, if you destabilize the top-down regulating influence of culture within a small group of peers, energetic nonlinear tribal organizations will spontaneously emerge within those groups. History has demonstrated that if you sprinkle LSD over a city then flower children will blossom and begin to reproduce. But close observation of modern psychedelic subcultures reveals that radical identity reinvention is not a function of spiritual freedom or political subversion, but is more a viral form of tribal bonding and indoctrination. For example, the hippies of 1960s and the ravers of 1990s each preached freedom and individuality, yet each culture had strictly controlled tribal uniforms, politics, musical styles, rituals, and so on, and ostracized outsiders as being squares or un-hip. This indicates that psychedelic identity reinvention is not a function of freedom of expression or social liberation, but is instead driven by the typical rewards of social elitism, the fears of being ostracized, and the reinforcements of tribal acceptance; all of which strongly affect identity-based neuroplasticity. Presumably any tribe, cultural group, religion, cult, or government can employ psychedelic neuroplasticity to similar social organizing effect.
 LeDoux, Joseph, 'Synaptic Self'. Viking Penguin, NY, 2002.
 Griffiths, R.R., 'Psilocybin can occasion mystical-type experiences having substantial and sustained personal meaning and spiritual significance'. Psychopharmacology (2006) 187:268–283
 Observations of individuals adopting new names and new identities in response to psychedelic indoctrination come from subjective reports and first-hand observations of psychedelic subcultures.
 Gresch PJ, Smith RL, Barrett RJ, Sanders-Bush E., 'Behavioral tolerance to lysergic acid diethylamide is associated with reduced serotonin-2A receptor signaling in rat cortex.'. Neuropsychopharmacology. 2005 Sep;30(9):1693-702.
 Abraham HD, Duffy FH, 'EEG coherence in post-LSD visual hallucinations'. Psychiatry Res. 2001 Oct 1;107(3):151-63.
 Groups linked to the weaponized use of psychedelics include the Manson Family, the SLA, Aum Shinrikyo, the CIA, and the United States Department of Defense.
 Hobson, J. Allan, 'The Dream Drugstore: Chemically Altered States of Consciousness'. MIT Press, 2001.
 Accounts of psychedelics producing a "screen saver" or hypnotic autopilot of unresolved anxieties and salient attractors are taken from subjective reports and surveys of psychedelic literature.
 Beyer, SV, 'Singing to the Plants: A Guide to Mestizo Shamanism in the Upper Amazon'. University of New Mexico Press (October 31, 2009)
 Reports of psychedelics facilitating symptoms of persistent psychosis taken from subjective reports and a survey of psychedelic overdose case studies.
 Shema R, Sacktor TC, Dudai Y, 'Rapid erasure of long-term memory associations in the cortex by an inhibitor of PKM zeta'. Science. 2007 Aug 17;317(5840):951-3.
 Bohn LM, 'Mitogenic Signaling via Endogenous κ-Opioid Receptors in C6 Glioma Cells: Evidence for the Involvement of Protein Kinase C and the Mitogen-Activated Protein Kinase Signaling Cascade'. J Neurochem. 2000 February; 74(2): 564–573.
 Ray TS, 'Psychedelics and the Human Receptorome'. PLoS One. 2010; 5(2): e9019.
 Nichols DE, 'Hallucinogens'. Pharmacology & Therapeutics Volume 101, Issue 2, February 2004, Pages 131-181
 Nichols CD, Sanders-Bush E, 'A Single Dose of Lysergic Acid Diethylamide Influences Gene Expression Patterns within the Mammalian Brain'. Neuropsychopharmacology (2002) 26 634-642
Citation: Kent, James L. Psychedelic Information Theory: Shamanism in the Age of Reason, Chapter 12, 'Psychedelic Neuroplasticity'. PIT Press, Seattle, 2010.
Copyright: © James L. Kent, 2010. Some Rights Reserved. Please read copyright information before reproducing.