PCE

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PCE may cause psychosis and mania at a significantly higher rate than other dissociatives.[1][2]

It is strongly discouraged to use this substance in high doses or multiple days in a row. Please see this section for more details.

Summary sheet: PCE
PCE
Molecular structure of Eticyclidine
PCE.svg
Chemical Nomenclature
Common names PCE, Eticyclidine
Substitutive name Eticyclidine
Systematic name (1-Phenylcyclohexyl)ethylamine
Class Membership
Psychoactive class Dissociative
Chemical class Arylcyclohexylamine
Routes of Administration

WARNING: Always start with lower doses due to differences between individual body weight, tolerance, metabolism, and personal sensitivity. See responsible use section.


Smoked
Dosage
Threshold 1 - 2 mg
Light 2 - 4 mg
Common 4 - 8 mg
Strong 8 - 12 mg
Heavy 12 mg+ Heavy doses may result in psychosis and mania.[3]
Duration
Total 4 - 6 hours
Onset 2 - 20 minutes
Come up 20 - 40 minutes
Peak 2 - 3 hours
Offset 1 - 2 hours
After effects 4 - 48 hours
Oral
Dosage
Threshold 1 - 3 mg
Light 3 - 5 mg
Common 5 - 10 mg
Strong 10 - 15 mg
Heavy 15mg+ Heavy doses may result in psychosis and mania.[4]
Duration
Total 4 - 8 hours
Onset 30 - 90 minutes
Come up 40 - 120 minutes
Peak 2 - 3 hours
Offset 1 - 2 hours
After effects 4 - 48 hours



Insufflated
Dosage
Threshold 1 - 2 mg
Light 2 - 4 mg
Common 4 - 8 mg
Strong 8 - 15 mg
Heavy 15mg+ Heavy doses may result in psychosis and mania.[5]
Duration
Total 4 - 6 hours
Onset 3 - 30 minutes
Come up 30 - 90 minutes
Peak 2 - 3 hours
Offset 1 - 2 hours
After effects 4 - 48 hours






DISCLAIMER: PW's dosage information is gathered from users and resources for educational purposes only. It is not a recommendation and should be verified with other sources for accuracy.

PCE (also known as Eticyclidine or CI-400) is a synthetic dissociative substance of the arylcyclohexylamine chemical class that produces dissociative, anesthetic and hallucinogenic effects when administered. Like its closely related structural analog PCP, PCE primarily exerts its effect as an NMDA receptor antagonist, where it noncompetitively binds to and blocks the activity of the NMDA receptor.[6][7][8]

PCP was marketed in the 1950s as an anesthetic pharmaceutical drug but was taken off the market in 1965 due to the high prevalence of dissociative hallucinogenic side effects, which was also discovered of PCE. Soon after, ketamine was discovered by Parke-Davis researchers as a better-tolerated derivative for use as an anesthetic pharmaceutical drug. Since this time, a number of synthetic derivatives of PCP have been sold as dissociative drugs for recreational and non-medical use.[9]

Today, PCE is typically taken as a recreational drug or more rarely, for entheogenic purposes alongside its popular contemporary relatives 3-MeO-PCP and 3-MeO-PCE. PCE may be ingested orally, smoked, insufflated or injected.[10] It has been noted for its potency, diversity in effects, long-lived effects, and abuse liability. Notably, PCE is slightly more potent than PCP and has similar effects, but its unpleasant taste and tendency to cause nausea made it less accepted by users, making it relatively obscure.

Chemistry

PCE, or Eticyclidine, is a synthetic dissociative of the arylcyclohexylamine class. PCE contains cyclohexane, a six-member saturated ring, bonded to a ring and -ethyl group at R1. One of these rings is a piperidine ring, a nitrogenous six member ring, bonded at its nitrogen group. The other constituent at the nitrogen is not a full cyclohexane ring like with PCP, but an ethyl group. As with PCP, PCE is an initialism named from the first letters of the three constituent rings phenyl, cyclohexane and ethyl.

Pharmacology

Further information: NMDA receptor antagonist

NMDA receptors (a subtype of receptors for glutamate, which are the principle excitatory neurotransmitters in the nervous system) allow for electrical signals to pass between nerve cells in the brain and spinal column; for the signals to pass, the receptor must be open. NMDA receptor antagonists have been shown to disrupt this signaling by blocking these receptors. This disconnection of information flow in the nervous system leads to loss of sensation (anesthesia), difficulty moving (motor discoordination), and eventually this substance's equivalent of a “"hole"-like state that is most associated with that experienced on ketamine, although of a qualitatively different nature.”[citation needed]

In addition to its unique NMDA receptor blocking abilities, PCE also acts as a dopamine-noradrenaline reuptake inhibitor as well a serotonin reuptake inhibitor with suspected µ-opioid affinity and typical dissociative effects. This provides an explanation for its euphoric and often stimulating properties.

Subjective effects

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This subjective effect breakdown is a stub.

As such, it may contain incomplete or wrong information and is still in progress.

You can help by expanding it.

The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects should be taken with a grain of salt and will rarely (if ever) occur all at once, but heavier doses will increase the chances and are more likely to induce a full range of effects. Likewise, adverse effects become much more likely on higher doses and may include injury or death.

Disconnective effects
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Visual effects
Eye.svg

Cognitive effects
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Toxicity and harm potential

The long-term use of PCE may lead to schizophrenia-like psychotic episodes, severe lasting memory loss, disorganized thinking, depression, weight loss, liver abnormalities and rhabdomyolysis (skeletal muscle breakdown).[13]

It is strongly recommended that one use harm reduction practices, such as volumetric dosing, when using this substance to ensure the administration of the intended dose.

Psychosis

PCE has been reported to cause psychosis and mania at a significantly higher rate than other dissociatives such as ketamine, diphenidine, or MXE. Multiple scientific papers describe states of psychosis, mania, and/or delirium occurring after moderate to large doses of the drug were ingested. In one initial human trial, it was reported that one-sixth of the patients who had received anesthetic doses became psychotic.[14] In some cases, it took up to a week or more to resolve. Similar results (although less severe) were reported during trials using subanesthetic doses of PCE for pain relief.[15]

It is strongly recommended that one use extreme caution and harm reduction practices when using this drug.

  • Users should avoid taking the drug multiple days in a row or becoming addicted to it as this increases the risk of severe adverse effects.
  • The recommended dosage range should not be exceeded as high doses can trigger adverse effects.
  • Users should start with extremely low doses and work their way up as slowly as possible. Volumetric liquid dosing should preferably be used due to the drug's potency; most standard milligram scales cannot accurately weigh out doses below 10-15mg.
  • Compulsive redosing before one has fully sobered up is not recommended and can result in too high of a dose.

Due to the risk of psychosis, it is not recommended to combine this drug with other substances, especially stimulants, psychedelics, or other dissociatives like MXE. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

Tolerance and addiction potential

The chronic use of PCE can be considered highly addictive with a high potential for adverse side effects such as psychosis. In comparison to other dissociatives, PCE has been reported to be more addictive than MXE, diphenidine, ephenidine, and ketamine. When addiction has developed, cravings and withdrawal effects may occur if a person suddenly stops their usage. There have been multiple reports across the internet of people becoming seriously addicted daily users of this substance so serious precautions and considerations should be taken before trying this substance.

Tolerance to many of the effects of PCE develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). PCE presents cross-tolerance with all dissociatives, meaning that after the consumption of PCE, all dissociatives will have a reduced effect.

Neurological effects

Some studies found that, like other NMDA receptor antagonists, PCE can cause brain damage called Olney's lesions in rats.[16][17] Studies conducted on rats showed that high doses of the NMDA receptor antagonist dizocilpine caused reversible vacuoles to form in certain regions of the rats' brains. All studies of Olney's lesions have only been performed on non-human animals and may not apply to humans. One unpublished study by Frank Sharp reportedly showed no damage by the NDMA antagonist ketamine (a similar drug) far beyond recreational doses[18] but its validity is controversial since it was never published.

PCE has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate levels in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[19] It also induces symptoms in humans that mimic schizophrenia.[20]

Urinary tract effects

In terms of its long-term health effects when used repeatedly and excessively for extended periods of time, PCE seems to exhibit similar extreme bladder and urinary tract problems to those found with other arylcyclohexylamines like ketamine or PCP.

  • Urinary frequency - Urinary frequency is the need to empty the bladder every few minutes.
  • Urinary urgency - This can be described as a sudden, compelling need to urinate.
  • Urinary pressure - This is experienced as a constant sensation of fullness in the bladder that is unrelieved by urination.
  • Pelvic and bladder pain - Pain can develop suddenly and severely, particularly as the bladder fills with urine.
  • Hematuria - Hematuria is visible blood in the urine.
  • Incontinence - This is the leakage of urine.

A large body of anecdotal evidence suggests that these symptoms can be minimized by not using PCE on a regular basis (daily or weekly at the bare minimum) and carefully monitoring and limiting one's usage of the substance, although general usage of this substance is still discouraged due to its observed toxic properties.

Dangerous interactions

Although many psychoactive substances are safe on their own, they can become dangerous and even life-threatening when combined with other substances. The list below contains some common potentially dangerous combinations, but may not include all of them. Certain combinations may be safe in low doses of each but still increase the potential risk of death. Independent research should always be done to ensure that a combination of two or more substances is safe before consumption.

  • Psychedelics - This combination is not advised because PCE has been reported to cause extreme psychological disturbances such as psychosis and mania at a significantly higher rate than other dissociatives.
  • Stimulants - This combination can potentiate the anxiety-inducing, manic, delusional and disinhibiting aspects of dissociatives, particularly those without pronounced motor and consciousness-suppression components like ketamine as this can increase the likelihood of a panic event or psychotic episode.
Prominent examples include PCP and its analogs 3-MeO-PCP, MXE, and the diarylethylamine dissociatives like diphenidine or ephenidine. There is also evidence that suggests that combining these two increases their neurotoxicity.[citation needed] Anecdotally, worsened comedowns are also commonly reported when these two classes of substances are combined.
  • Depressants - Because both depress the respiratory system, this combination can result in an increased risk of suddenly falling unconscious, vomiting and choking to death from the resulting suffocation. If nausea or vomiting occurs, users should attempt to fall asleep in the recovery position or have a friend move them into it.

Legality

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This legality section is a stub.

As such, it may contain incomplete or wrong information. You can help by expanding it.

  • Canada - PCE is Schedule I in Canada.[citation needed]
  • New Zealand - PCE is Schedule I (class A) in New Zealand.[citation needed]
  • Poland - PCE is Schedule II (II-P group) in Poland.[citation needed]
  • Portugal - Effective July 2001, personal use of PCE was decriminalized by Law 30/2000. Possession of less than 100 mg is not regarded as a criminal offence, although the substance is liable to be seized and the possessor can be referred to mandatory treatment. Sale or possession of quantities greater than the personal possession limit are criminal offences punishable by jail time.[citation needed]
  • United Kingdom - PCE is a class A in the U.K., making it illegal to buy or possess without a prescription.[citation needed]
  • United States - PCE is a Schedule II controlled substance.[citation needed]

See also

External links

Literature

  • Morris, H., & Wallach, J. (2014). From PCP to MXE: A comprehensive review of the non-medical use of dissociative drugs. Drug Testing and Analysis, 6(7–8), 614–632. https://doi.org/10.1002/dta.1620

References

  1. http://archives.drugabuse.gov/pdf/monographs/21.pdf | Luisada, Paul V., M.D. "The Phencyclidine Psychosis: Phenomenology and Treatment." Phencyclidine (PCP) Abuse: An Appraisal. Rockville, Maryland: National Institute on Drug Abuse, 1978. pg. 241.
  2. Tasman, Allan, Jerald Kay, and Jeffrey A. Lieberman. Psychiatry. Chichester: John Wiley & Sons, 2003. Google Books. Wiley. Web. <https://books.google.com/books?id=l2KRBgAAQBAJ&pg=PT4957&lpg=PT4957&dq=Greifenstein+et+al.+1958%29.&source=bl&ots=s5CFdAfMzc&sig=GzsOq_N-V1qtahxyyHnKMJceEj0&hl=en&sa=X&ved=0ahUKEwji0pWTjNLKAhUBaD4KHTfqD0sQ6AEIHDAA#v=onepage&q=Greifenstein%20et%20al.%201958%29.&f=false>.
  3. PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
  4. PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
  5. 3-MeO-PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
  6. From PCP to MXE: a comprehensive review of the non-medical use of dissociative drugs (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/24678061
  7. Drugs and Behavior, 4th Edition, McKim, William A., ISBN 0-13-083146-8
  8. NMDA receptor antagonists ketamine and PCE have direct effects on the dopamine D2 and serotonin 5-HT2receptors¾implications for models of schizophrenia | http://www.nature.com/mp/journal/v7/n8/full/4001093a.html
  9. From PCE to MXE: a comprehensive review of the non-medical use of dissociative drugs (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/24678061
  10. http://drugabuse.gov/infofacts/hallucinogens.html
  11. http://archives.drugabuse.gov/pdf/monographs/21.pdf | Luisada, Paul V., M.D. "The Eticyclidine Psychosis: Phenomenology and Treatment." Eticyclidine (PCE) Abuse: An Appraisal. Rockville, Maryland: National Institute on Drug Abuse, 1978. pg. 241.
  12. Tasman, Allan, Jerald Kay, and Jeffrey A. Lieberman. Psychiatry. Chichester: John Wiley & Sons, 2003. Google Books. Wiley. Web. <https://books.google.com/books?id=l2KRBgAAQBAJ&pg=PT4957&lpg=PT4957&dq=Greifenstein+et+al.+1958%29.&source=bl&ots=s5CFdAfMzc&sig=GzsOq_N-V1qtahxyyHnKMJceEj0&hl=en&sa=X&ved=0ahUKEwji0pWTjNLKAhUBaD4KHTfqD0sQ6AEIHDAA#v=onepage&q=Greifenstein%20et%20al.%201958%29.&f=false>.
  13. PCE Effects by Erowid | https://www.erowid.org/chemicals/PCE/PCE_effects.shtml
  14. http://archives.drugabuse.gov/pdf/monographs/21.pdf | Luisada, Paul V., M.D. "The Eticyclidine Psychosis: Phenomenology and Treatment." Eticyclidine (PCE) Abuse: An Appraisal. Rockville, Maryland: National Institute on Drug Abuse, 1978. pg. 241.
  15. Tasman, Allan, Jerald Kay, and Jeffrey A. Lieberman. Psychiatry. Chichester: John Wiley & Sons, 2003. Google Books. Wiley. Web. <https://books.google.com/books?id=l2KRBgAAQBAJ&pg=PT4957&lpg=PT4957&dq=Greifenstein+et+al.+1958%29.&source=bl&ots=s5CFdAfMzc&sig=GzsOq_N-V1qtahxyyHnKMJceEj0&hl=en&sa=X&ved=0ahUKEwji0pWTjNLKAhUBaD4KHTfqD0sQ6AEIHDAA#v=onepage&q=Greifenstein%20et%20al.%201958%29.&f=false>.
  16. Pathological changes induced in cerebrocortical neurons by PCE and related drugs (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/2660263
  17. Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/7976530
  18. Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0-9660019-7-4
  19. Chronic PCE administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/15653257
  20. Eticyclidine (PCE): a dangerous drug, but useful in schizophrenia research (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/12206280