
PCE: Difference between revisions
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{{distinguish2|[[PCP]] (Phencyclidine)}} | |||
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| ''[[PCE/Summary|Summary sheet: PCE]]'' | | ''[[PCE/Summary|Summary sheet: PCE]]'' | ||
|}'''PCE''' (also known as '''Eticyclidine''' or '''CI-400''') is a synthetic [[psychoactive class::dissociative]] of the [[chemical class::arylcyclohexylamine]] class that produces [[anesthetic]] and [[hallucinogenic]] effects. It is a close analog of the classic synthetic | |}'''PCE''' (also known as '''Eticyclidine''' or '''CI-400''') is a synthetic [[psychoactive class::dissociative]] of the [[chemical class::arylcyclohexylamine]] class that produces [[anesthesia|anesthetic]] (i.e. pain-blocking) and [[hallucinogenic]] effects. It is a close analog of the classic synthetic anesthetic [[PCP]]. Like PCP, PCE exerts is effect primarily as an [[NMDA receptor antagonist]], where it noncompetitively binds to and blocks the activity of the NMDA receptor, which is a type of glutamate receptor essential for excitatory neurotransmission throughout the brain. Like PCP, PCE is associated with compulsive abuse, although it is significantly more obscure.<ref>Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 374–375. ISBN 9780071481274. </ref><ref>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</ref><ref>Drugs and Behavior, 4th Edition, McKim, William A., ISBN 0-13-083146-8</ref><ref>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</ref> | ||
PCP was marketed in the 1950s as an [[Pain relief|anesthetic]] pharmaceutical drug but was taken off the market in 1965 due to the high prevalence of dissociative [[hallucinogen]]ic side effects, which was also discovered of PCE. Likewise [[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.<ref>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</ref> | PCP was marketed in the 1950s as an [[Pain relief|anesthetic]] pharmaceutical drug but was taken off the market in 1965 due to the high prevalence of dissociative [[hallucinogen]]ic side effects, which was also discovered of PCE. Likewise [[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.<ref>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</ref> | ||
In modern times, PCE is typically ingested as a recreational drug or more rarely, for [[entheogen]]ic purposes as are its popular contemporary relatives [[3-MeO-PCP]] and [[3-MeO-PCE]]. PCE may be ingested [[orally]], [[Routes of administration#Smoking|smoked]], [[insufflated]] or [[Routes of administration#Injection|injected]].<ref>http://drugabuse.gov/infofacts/hallucinogens.html</ref> and is noted for its potency, diversity in effects, and long-lasting nature. 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 relativley obscure. | |||
In modern times, PCE is typically ingested as a recreational drug or more rarely, for [[entheogen]]ic purposes as are its popular contemporary relatives [[3-MeO-PCP]] and [[3-MeO-PCE]]. PCE may be ingested [[orally]], [[Routes of administration#Smoking|smoked]], [[insufflated]] or [[Routes of administration#Injection|injected]].<ref>http://drugabuse.gov/infofacts/hallucinogens.html</ref> and is noted for its potency, diversity in effects, and long-lasting nature. | |||
==Chemistry== | ==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 R<sub>1</sub>. 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. PCE is an initialism named from the first letters of the three constituent rings '''p'''henyl, '''c'''yclohexane and '''e''thyl | 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 R<sub>1</sub>. 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 '''p'''henyl, '''c'''yclohexane and '''e'''thyl. | ||
==Pharmacology== | ==Pharmacology== | ||
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===Visual effects=== | ===Visual effects=== | ||
====Suppression==== | ====Suppression==== | ||
*'''[[Effect::Visual disconnection]]''' - This eventually results in PCE's equivalent of the | *'''[[Effect::Visual disconnection]]''' - This eventually results in PCE's equivalent of the "k-hole" or more specifically, ''[[Visual disconnection#Holes, spaces and voids|holes, spaces and voids]]'' alongside of ''[[Visual disconnection#Structures|structures]]''. However, unlike ketamine, PCE does not immobilize the user at this level, which can lead to unpredictable psychotic behavior. | ||
*'''[[Effect::Visual acuity suppression]]''' | *'''[[Effect::Visual acuity suppression]]''' | ||
*'''[[Effect::Double vision]]''' | *'''[[Effect::Double vision]]''' | ||
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==See also== | ==See also== | ||
*[[Responsible use]] | *[[Responsible use]] | ||
*[[Research chemical]] | |||
*[[Dissociative]] | *[[Dissociative]] | ||
*[[PCP]] | *[[PCP]] | ||
*[[MXE]] | *[[MXE]] | ||
*[[ | *[[3-MeO-PCE]] | ||
==External links== | ==External links== | ||
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*[https://www.erowid.org/chemicals/PCE/ PCE (Erowid)] | *[https://www.erowid.org/chemicals/PCE/ PCE (Erowid)] | ||
*[http://factsheet.tripsit.me/PCE PCE TripSit] | *[http://factsheet.tripsit.me/PCE PCE TripSit] | ||
* | |||
==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== | ==References== | ||
<references /> | <references /> | ||
[[Category:Psychoactive substance]] | |||
[[Category:Psychoactive substance]][[Category:Arylcyclohexylamine]][[Category:Dissociative]][[Category:Research chemical]] | [[Category:Arylcyclohexylamine]] | ||
[[Category:Dissociative]] | |||
[[Category:Research chemical]] | |||
{{#set:Featured=true}} |
Revision as of 17:11, 9 April 2017
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.
This page has not been fully approved by the PsychonautWiki administrators. It may contain incorrect information, particularly with respect to dosage, duration, subjective effects, toxicity and other risks. It may also not meet PW style and grammar standards. |
PCE | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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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 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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Interactions | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Stimulants | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Depressants |
Summary sheet: PCE |
PCE (also known as Eticyclidine or CI-400) is a synthetic dissociative of the arylcyclohexylamine class that produces anesthetic (i.e. pain-blocking) and hallucinogenic effects. It is a close analog of the classic synthetic anesthetic PCP. Like PCP, PCE exerts is effect primarily as an NMDA receptor antagonist, where it noncompetitively binds to and blocks the activity of the NMDA receptor, which is a type of glutamate receptor essential for excitatory neurotransmission throughout the brain. Like PCP, PCE is associated with compulsive abuse, although it is significantly more obscure.[6][7][8][9]
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. Likewise 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.[10]
In modern times, PCE is typically ingested as a recreational drug or more rarely, for entheogenic purposes as are its popular contemporary relatives 3-MeO-PCP and 3-MeO-PCE. PCE may be ingested orally, smoked, insufflated or injected.[11] and is noted for its potency, diversity in effects, and long-lasting nature. 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 relativley 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
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 effects section is a stub. As such, it is still in progress and may contain incomplete or wrong information. You can help by expanding or correcting it. |
The effects listed below are based upon the subjective effects index and personal experiences of PsychonautWiki contributors. The listed effects will rarely (if ever) occur all at once, but heavier dosages will increase the chances and are more likely to induce a full range of effects.
PCE is considerably more likely to induce psychosis than other dissociatives and is therefore potentially dangerous regardless of setting.
Physical effects
- Tactile disconnection
- Spontaneous tactile sensations
- Tactile suppression
- Physical autonomy
- Motor control loss
- Physical euphoria
- Perception of decreased weight
- Dizziness
- Nausea
- Visual sliding
Cognitive effects
The general head space of PCE is often described as particularly stimulating, euphoric and clear-headed in comparison to that of DXM and ketamine. The specific cognitive effects can be broken down into several separate subcomponents which are listed and described below:
- Psychosis - This effect is more common on PCE than other dissociatives.[1][2]
- Delusions
- Depersonalization
- Derealization
- Consciousness disconnection
- Memory suppression
- Thought acceleration
- Immersion enhancement
- Information processing suppression
- Time distortion
- Euphoria
- Introspection
- Déjà vu
- Conceptual thinking
- Compulsive redosing
- Anxiety suppression
- Disinhibition
- Amnesia
- Feelings of impending doom
- Creativity enhancement
Visual effects
Suppression
- Visual disconnection - This eventually results in PCE's equivalent of the "k-hole" or more specifically, holes, spaces and voids alongside of structures. However, unlike ketamine, PCE does not immobilize the user at this level, which can lead to unpredictable psychotic behavior.
- Visual acuity suppression
- Double vision
- Pattern recognition suppression
- Frame rate suppression
Distortions
Hallucinatory states
At high doses, PCE can produce a full range of high-level hallucinatory states in a fashion that is less consistent and reproducible than that of many other commonly used psychedelics. These effects include:
Auditory effects
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).[12]
It is strongly recommended that one use harm reduction practices when using this drug.
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.[1] 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.[2]
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 [[Cross-tolerance::all dissociatives]], meaning that after the consumption of PCE, all dissociatives will have a reduced effect.
Brain effects
Some studies found that, like other NMDA receptor antagonists, PCE can cause brain damage called Olney's lesions in rats.[13][14] 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[15] 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.[16] It also induces symptoms in humans that mimic schizophrenia.[17]
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
Warning: Many psychoactive substances that are reasonably safe to use on their own can suddenly become dangerous and even life-threatening when combined with certain other substances. The following list provides some known dangerous interactions (although it is not guaranteed to include all of them).
Always conduct independent research (e.g. Google, DuckDuckGo, PubMed) to ensure that a combination of two or more substances is safe to consume. Some of the listed interactions have been sourced from TripSit.
- 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.[1][2]
- Stimulants - This combination is not advised due to the risk of psychosis or mania.[1][2]
- Stimulants - Both stimulants and dissociatives carry the risk of adverse psychological reactions like anxiety, mania, delusions and psychosis and these risks are exacerbated when the two 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.
Legal issues
- Canada - PCE is Schedule I in Canada.
- New Zealand - PCE is Schedule I (class A) in New Zealand.
- Poland - PCE is Schedule II (II-P group) in Poland.
- 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.
- U.K. - PCE is a class A in the U.K., making it illegal to buy or possess without a prescription.
- U.S. - PCE is a Schedule II controlled substance.
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
- ↑ 1.0 1.1 1.2 1.3 1.4 Luisada, P. V. M. D. (1978), The Phencyclidine Psychosis: Phenomenology and Treatment." Phencyclidine (PCP) Abuse: An Appraisal., National Institute on Drug Abuse Cite error: Invalid
<ref>
tag; name "one" defined multiple times with different content - ↑ 2.0 2.1 2.2 2.3 2.4 Tasman, A., Kay, J., Lieberman, J. A., First, M. B., Riba, M. (5 February 2015). Psychiatry. John Wiley & Sons. ISBN 9781118753361. Cite error: Invalid
<ref>
tag; name "two" defined multiple times with different content - ↑ PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
- ↑ PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
- ↑ 3-MeO-PCP Psychosis (PsychonautWiki) | https://psychonautwiki.org/wiki/3-MeO-PCP#Toxicity_and_harm_potential
- ↑ Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 374–375. ISBN 9780071481274.
- ↑ 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
- ↑ Drugs and Behavior, 4th Edition, McKim, William A., ISBN 0-13-083146-8
- ↑ 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
- ↑ 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
- ↑ http://drugabuse.gov/infofacts/hallucinogens.html
- ↑ PCE Effects by Erowid | https://www.erowid.org/chemicals/PCE/PCE_effects.shtml
- ↑ Pathological changes induced in cerebrocortical neurons by PCE and related drugs (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/2660263
- ↑ 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
- ↑ Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0-9660019-7-4
- ↑ 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
- ↑ Eticyclidine (PCE): a dangerous drug, but useful in schizophrenia research (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/12206280