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===Brain effects===
===Brain effects===
Some studies found that, like other [[NMDA receptor antagonist]]s, phencyclidine can cause a certain kind of [[brain damage]] called [[Olney's lesions]] in rats.<ref>{{cite journal |author=Olney J, Labruyere J, Price M |title=Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs |journal=Science |volume=244 |issue=4910 |pages=1360–1362 |year=1989 |pmid=2660263 | doi = 10.1126/science.2660263}}</ref><ref>{{cite journal |author=Hargreaves R, Hill R, Iversen L |title=Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology |journal=Acta Neurochir Suppl (Wien) |volume=60 |issue= |pages=15–9 |year= 1994|pmid=7976530}}</ref> Studies conducted on rats showed that high doses of the NMDA receptor antagonist [[dizocilpine|MK-801]] caused reversible [[vacuole]]s to form in certain regions of the rats' brains. All studies of Olney's lesions have only been performed on animals and may not apply to humans. The research into the relationship between rat brain metabolism and the creation of Olney's Lesions has been discredited and may not apply to humans, as has been shown with ketamine.<ref>Jansen, Karl. ''Ketamine: Dreams and Realities.'' MAPS, 2004. ISBN 0-9660019-7-4</ref><ref>[http://www.erowid.org/chemicals/dxm/dxm_health3.shtml Erowid DXM Vault : Response to "The Bad News Isn't In": Please Pass The Crow, by William E. White<!-- Bot generated title -->]</ref>
Some studies found that, like other [[NMDA receptor antagonist]]s, phencyclidine can cause a certain kind of [[brain damage]] called [[Olney's lesions]] in rats.<ref>{{cite journal |author=Olney J, Labruyere J, Price M |title=Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs |journal=Science |volume=244 |issue=4910 |pages=1360–1362 |year=1989 |pmid=2660263 | doi = 10.1126/science.2660263}}</ref><ref>{{cite journal |author=Hargreaves R, Hill R, Iversen L |title=Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology |journal=Acta Neurochir Suppl (Wien) |volume=60 |issue= |pages=15–9 |year= 1994|pmid=7976530}}</ref> Studies conducted on rats showed that high doses of the NMDA receptor antagonist [[dizocilpine|MK-801]] caused reversible [[vacuole]]s to form in certain regions of the rats' brains. All studies of Olney's lesions have only been performed on animals and may not apply to humans. The research into the relationship between rat brain metabolism and the creation of Olney's Lesions has been discredited and may{{Weasel-inline|date=May 2011}} not apply to humans, as has been shown with ketamine.<ref>Jansen, Karl. ''Ketamine: Dreams and Realities.'' MAPS, 2004. ISBN 0-9660019-7-4</ref><ref>[http://www.erowid.org/chemicals/dxm/dxm_health3.shtml Erowid DXM Vault : Response to "The Bad News Isn't In": Please Pass The Crow, by William E. White<!-- Bot generated title -->]</ref>


Phencyclidine has also been shown to cause [[schizophrenia]]-like changes in ''N''-acetylaspartate and ''N''-acetylaspartylglutamate in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.<ref name=psychotic_PCP_rats>{{cite journal | last = Reynolds | first = Lindsay M. | coauthors = Susan M. Cochran, Brian J. Morris, Judith A. Pratt and Gavin P. Reynolds | date = March 1, 2005 | title = Chronic phencyclidine administration induces schizophrenia-like changes in ''N''-acetylaspartate and ''N''-acetylaspartylglutamate in rat brain | journal = Schizophrenia Research | volume = 73 | issue = 2-3 | pages = 147–152 | doi = 10.1016/j.schres.2004.02.003 | pmid = 15653257 | accessdate = 2006-09-29}}</ref> It also induces symptoms in humans that mimic schizophrenia.<ref>{{cite journal |doi=10.1080/00223980209604159 |author=Murray JB |title=Phencyclidine (PCP): a dangerous drug, but useful in schizophrenia research |journal=J Psychol |volume=136 |issue=3 |pages=319–327 |year=2002 |month=May |pmid=12206280}}</ref>
Phencyclidine has also been shown to cause [[schizophrenia]]-like changes in ''N''-acetylaspartate and ''N''-acetylaspartylglutamate in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.<ref name=psychotic_PCP_rats>{{cite journal | last = Reynolds | first = Lindsay M. | coauthors = Susan M. Cochran, Brian J. Morris, Judith A. Pratt and Gavin P. Reynolds | date = March 1, 2005 | title = Chronic phencyclidine administration induces schizophrenia-like changes in ''N''-acetylaspartate and ''N''-acetylaspartylglutamate in rat brain | journal = Schizophrenia Research | volume = 73 | issue = 2-3 | pages = 147–152 | doi = 10.1016/j.schres.2004.02.003 | pmid = 15653257 | accessdate = 2006-09-29}}</ref> It also induces symptoms in humans that mimic schizophrenia.<ref>{{cite journal |doi=10.1080/00223980209604159 |author=Murray JB |title=Phencyclidine (PCP): a dangerous drug, but useful in schizophrenia research |journal=J Psychol |volume=136 |issue=3 |pages=319–327 |year=2002 |month=May |pmid=12206280}}</ref>


The full extent of the pharmacology of this compound in the human CNS is not fully understood; it binds to many different receptor sites. The primary interactions are as a non-competitive antagonist at the 3A-subunit [epsilon subunit] of the NMDA receptor.{{Citation needed|date=July 2011}} Phencyclidine is known to bind, with relatively high affinity, to the D1 subunit of the human '''DAT''' (Dopamine Transporter){{Citation needed|date=July 2011}}, in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR).{{Citation needed|date=July 2011}} It also binds to the mu-opioid receptor{{Citation needed|date=July 2011}}, which seems to be a central part of the mechanism of action of drugs in this class.{{Citation needed|date=July 2011}} (For example, Dizocilpine [MK-801] shows little appreciable analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits – this may well be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR may play a role in transmission of pain signals).{{Citation needed|date=July 2010}}
The full extent of the pharmacology of this compound in the human CNS is not fully understood; it binds to many different receptor sites. The primary interactions are as a non-competitive antagonist at the 3A-subunit [epsilon subunit] of the NMDA receptor.{{Citation needed|date=July 2011}} Phencyclidine is known{{By whom|date=May 2011}} to bind, with relatively high affinity, to the D1 subunit of the human '''DAT''' (Dopamine Transporter){{Citation needed|date=July 2011}}, in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR).{{Citation needed|date=July 2011}} It also binds to the mu-opioid receptor{{Citation needed|date=July 2011}}, which seems {{Weasel-inline|date=May 2011}} to be a central part of the mechanism of action of drugs in this class.{{Citation needed|date=July 2011}} (For example, Dizocilpine [MK-801] shows little appreciable {{Weasel-inline|date=May 2011}} analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits – this may well {{Weasel-inline|date=May 2011}} be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR may {{Weasel-inline|date=May 2011}} play a role in transmission of pain signals).{{Citation needed|date=July 2010}}


===History and medicinal use===
===History and medicinal use===

Revision as of 01:04, 24 July 2011

Phencyclidine
Clinical data
Routes of
administration		Smoked, Insufflated, Oral
ATC code
  • none
Legal status
Legal status
Pharmacokinetic data
Elimination half-life7–46 hours
Identifiers
  • 1-(1-phenylcyclohexyl)piperidine
CAS Number
PubChem CID
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.150.427 Edit this at Wikidata
Chemical and physical data
FormulaC17H25N
Molar mass243.387 g/mol g·mol−1
3D model (JSmol)
  • c1ccccc1C3(N2CCCCC2)CCCCC3
  • InChI=1S/C17H25N/c1-4-10-16(11-5-1)17(12-6-2-7-13-17)18-14-8-3-9-15-18/h1,4-5,10-11H,2-3,6-9,12-15H2 checkY
  • Key:JTJMJGYZQZDUJJ-UHFFFAOYSA-N checkY
Data page
Phencyclidine (data page)
  (verify)

Phencyclidine (a complex clip of the chemical name 1-(1-phenylcyclohexyl)piperidine), commonly initialized as PCP and known colloquially as angel dust, is a recreational dissociative drug. Formerly used as an anesthetic agent, PCP exhibits both hallucinogenic and neurotoxic effects.[1]

First synthesized in 1926,[2] it was eventually patented in 1952 by the Parke-Davis pharmaceutical company and marketed under the brand name Sernyl. In chemical structure, PCP is an arylcyclohexylamine derivative, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA receptor and, like most antiglutamatergic hallucinogens, is significantly more dangerous than other categories of hallucinogens.[3][4] Other NMDA receptor antagonists include ketamine, tiletamine, dextromethorphan and nitrous oxide. Although the primary psychoactive effects of PCP last for a few hours, its total elimination rate from the body typically extends eight days or longer.

As a recreational drug, PCP may be ingested, smoked, or snorted.[5]

Biochemistry and pharmacology

Pharmacodynamics

PCP is well known for its primary action on ionotropic glutamate receptors, such as the NMDA receptor in rats and in rat brain homogenate.[6] [7] As such, PCP is an NMDA antagonist. NMDA receptors mediate excitation[8], however, studies have shown that PCP unexpectedly produces substantial cortical activation in humans[9] and rodents.[10]

Research also indicates that PCP inhibits nicotinic acetylcholine (nACh) receptors. Analogues of PCP exhibit varying potency at nACh receptors[citation needed] and NMDA receptors.[11] In some brain regions, these effects are believed [by whom?]to act synergistically by inhibiting excitatory activity.[citation needed]

PCP, like ketamine, also acts as a D2 receptor partial agonist in rat brain homogenate.[7] This activity may be associated with some of the more psychotic features of PCP intoxication, which is evidenced by the successful use of D2 receptor antagonists (such as haloperidol) in the treatment of PCP psychosis.[12]

The relative immunity to pain is likely produced by indirect interaction with the endogenous endorphin and enkephalin system, as has been suggested by studies involving rats.[13][clarification needed]

PCP is also believed[by whom?] to work as a dopamine reuptake inhibitor.[citation needed]

Pharmacokinetics

PCP is metabolized into PCHP, PPC and PCAA.

When smoked, some of it is broken down by heat into 1-phenyl-1-cyclohexene (PC) and piperidine.

Conversion of PCP into PC and piperidine by heat. (Image in the PD)

Structural analogues

Possible Analogues of PCP

More than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA. The best known of these are PCPy (rolicyclidine, 1-(1-phenylcyclohexyl)pyrrolidine); PCE (eticyclidine, N-ethyl-1-phenylcyclohexylamine); and TCP (tenocyclidine, 1-(1-(2-Thienyl)cyclohexyl)piperidine). These compounds were never widely-used and did not seem to be as well-accepted by users as PCP itself, however they were all added onto Schedule I of the Controlled Substance Act because of their putative similar effects.[14][citation needed]

The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP analogues, and summarized below. All of these analogues would have somewhat similar effects to PCP itself, although, with a range of potencies and varying mixtures of anesthetic, dissociative and stimulant effects depending on the particular substituents used. In some countries such as the USA, Australia, and New Zealand, all of these compounds would be considered controlled substance analogues of PCP, and are hence illegal drugs, even though many of them have never been made or tested.[15][16][clarification needed]

Brain effects

Some studies found that, like other NMDA receptor antagonists, phencyclidine can cause a certain kind of brain damage called Olney's lesions in rats.[17][18] Studies conducted on rats showed that high doses of the NMDA receptor antagonist MK-801 caused reversible vacuoles to form in certain regions of the rats' brains. All studies of Olney's lesions have only been performed on animals and may not apply to humans. The research into the relationship between rat brain metabolism and the creation of Olney's Lesions has been discredited and may[weasel words] not apply to humans, as has been shown with ketamine.[19][20]

Phencyclidine has also been shown to cause schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in the rat brain, which are detectable both in living rats and upon necropsy examination of brain tissue.[21] It also induces symptoms in humans that mimic schizophrenia.[22]

The full extent of the pharmacology of this compound in the human CNS is not fully understood; it binds to many different receptor sites. The primary interactions are as a non-competitive antagonist at the 3A-subunit [epsilon subunit] of the NMDA receptor.[citation needed] Phencyclidine is known[by whom?] to bind, with relatively high affinity, to the D1 subunit of the human DAT (Dopamine Transporter)[citation needed], in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR).[citation needed] It also binds to the mu-opioid receptor[citation needed], which seems [weasel words] to be a central part of the mechanism of action of drugs in this class.[citation needed] (For example, Dizocilpine [MK-801] shows little appreciable [weasel words] analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits – this may well [weasel words] be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR may [weasel words] play a role in transmission of pain signals).[citation needed]

History and medicinal use

PCP was first synthesized in 1926 and later tested after World War II as a surgical anesthetic. Because of its adverse side effects, such as hallucinations, mania, delirium, and disorientation, it was shelved until the 1950s. In 1953, it was patented by Parke-Davis and named Sernyl (referring to serenity),[23] but was only used in humans for a few years because of side-effects. In 1967, it was given the trade name Sernylan and marketed as a veterinary anesthetic, but was again discontinued. Its side effects and long half-life in the human body made it unsuitable for medical applications.

Recreational use

Illicit PCP seized by the DEA in several forms.

PCP began to emerge as a recreational drug in major cities in the United States in 1967.[24] In 1978, People magazine and Mike Wallace of 60 Minutes called PCP the country's "number one" drug problem. Although recreational use of the drug had always been relatively low, it began declining significantly in the 1980s. In surveys, the number of high school students admitting to trying PCP at least once fell from 13% in 1979 to less than 3% in 1990.[25]

PCP comes in both powder and liquid forms (PCP base is dissolved most often in ether), but typically it is sprayed onto leafy material such as cannabis, mint, oregano, parsley, or ginger leaves, then smoked.

PCP is a Schedule II substance in the United States, a List I drug of the Opium Law in the Netherlands and a Class A substance in the United Kingdom.

Methods of administration

In its pure (free base) form, PCP is a yellow oil (usually dissolved in petroleum, diethyl ether, or tetrahydrofuran). Upon treatment with hydrogen chloride gas, or isopropyl alcohol saturated with hydrochloric acid, this oil precipitates into white-tan crystals or powder (PCP hydrochloride). In this, the salt form, PCP can be insufflated, depending upon the purity. However, most PCP on the illicit market often contains a number of contaminants as a result of makeshift manufacturing, causing the color to range from tan to brown, and the consistency to range from powder to a gummy mass.[citation needed] These contaminants can range from unreacted piperidine and other precursors, to carcinogens like benzene and cyanide-like compounds such as PCC (piperidinocyclohexyl carbonitrile).[citation needed]

The term "embalming fluid" is often used to refer to the liquid PCP in which a cigarette is dipped, to be ingested through smoking, commonly known as "boat" or "water." The name most likely originated from the somatic "numbing" effect and feelings of dissociation induced by PCP, and has led to the widespread and mistaken belief that the liquid is made up of or contains real embalming fluid. Occasionally, however, some users and dealers could have, believing this myth, used real embalming fluid mixed with, or in place of, PCP.[26][27] Smoking PCP is known as "getting wet", and a cigarette or joint which has been dipped in PCP may be referred to on the street as a "fry stick," "sherm," "amp," "KJ (an abbreviation for 'Killer Joint')," "toe tag", "dipper", "happy stick," or "wet stick." "Getting wet" may have once been a popular method of using PCP, especially in the western United States where it may have been sold for about $10 to $25 per cigarette.[citation needed]

Effects

Behavioral effects can vary by dosage. Low doses produce a numbness in the extremities and intoxication, characterized by staggering, unsteady gait, slurred speech, bloodshot eyes, and loss of balance. Moderate doses (5–10 mg intranasal, or 0.01–0.02 mg/kg intramuscular or intravenous) will produce analgesia and anesthesia. High doses may lead to convulsions.[28] Frequently users do not know how much of the drug they are taking due to the tendency of the drug to be made illegally in uncontrolled conditions.[29]

Psychological effects include severe changes in body image, loss of ego boundaries, paranoia and depersonalization. Hallucinations, euphoria, suicidal impulses and aggressive behavior are reported.[28][30] The drug has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. Intoxicated individuals may act in an unpredictable fashion, possibly driven by their delusions and hallucinations. PCP may induce feelings of strength, power, and invulnerability as well as a numbing effect on the mind.[5] Occasionally, this leads to bizarre acts of violence.[31] However, studies by the Drug Abuse Warning Network in the 1970s show that media reports of PCP-induced violence are greatly exaggerated and that incidents of violence were unusual and often (but not always) limited to individuals with reputations for aggression regardless of drug use.[32] The reports in question often dealt with a supposed increase in strength imparted by the drug; this could partially be explained by the anaesthetic effects of the drug. The most commonly-cited types of incidents included self-mutilation of various types, breaking handcuffs (a feat reportedly requiring about 550 lbf (2.4 kN) of force), inflicting remarkable property damage, and pulling one's own teeth.[32][33][34]

Included in the portfolio of behavioral disturbances are acts of self-injury including suicide, and attacks on others or destruction of property. The analgesic properties of the drug can cause users to feel less pain, and persist in violent or injurious acts as a result. Recreational doses of the drug can also induce a psychotic state that resembles schizophrenic episodes which can last for months at a time with toxic doses.[35] Users generally report an "out-of-body" experience where they feel detached from reality, or one's consciousness seems somewhat disconnected from reality.[36]

Symptoms are summarized by the mnemonic device RED DANES: rage, erythema (redness of skin), dilated pupils, delusions, amnesia, nystagmus (oscillation of the eyeball when moving laterally), excitation, and skin dryness.[37]

Management of intoxication

Management of phencyclidine intoxication mostly consists of supportive care — controlling breathing, circulation, and body temperature — and, in the early stages, treating psychiatric symptoms.[38][39][40] Benzodiazepines, such as lorazepam, are the drugs of choice to control agitation and seizures (when present). Typical antipsychotics such as phenothiazines and haloperidol have been used to control psychotic symptoms, but may produce many undesirable side effects — such as dystonia — and their use is therefore no longer preferred; phenothiazines are particularly risky, as they may lower the seizure threshold, worsen hyperthermia, and boost the anticholinergic effects of PCP.[38][39] If an antipsychotic is given, intramuscular haloperidol has been recommended.[40][41][42]

Forced acid diuresis (with ammonium chloride or, more safely, ascorbic acid) may increase clearance of PCP from the body, and was somewhat controversially recommended in the past as a decontamination measure.[38][39][40] However, it is now known that only around 10% of a dose of PCP is removed by the kidneys, which would make increased urinary clearance of little consequence; furthermore, urinary acidification is dangerous, as it may induce acidosis and worsen rhabdomyolysis (muscle breakdown), which is not an unusual manifestation of PCP toxicity.[38][39]

See also

References

  1. ^ Maisto, Stephen A. (2004). Drug Use and Abuse. Thompson Wadsworth. ISBN 0-15-508517-4. {{cite book}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  2. ^ Development of PCP, 2006 ,CESAR (Center for Substance Abuse Research)
  3. ^ Drugs and Behavior, 4th Edition, McKim, William A., ISBN 0-13-083146-8
  4. ^ Kapur, S. and P. Seeman. "NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptorsimplications for models of schizophrenia(2002)
  5. ^ a b "NIDA InfoFacts: Hallucinogens - LSD, Peyote, Psilocybin, and PCP". DrugAbuse.gov. National Institute on Drug Abuse. Retrieved 2011-01-26.
  6. ^ Large, CH; Bison, S (2011). "The Efficacy of Sodium Channel Blockers to Prevent Phencyclidine-Induced Cognitive Dysfunction in the Rat: Potential for Novel Treatments for Schizophrenia". Journal of pharmacology and experimental therapeutics. 338 (1): 100-113 =. Retrieved July 2011. {{cite journal}}: Check date values in: |accessdate= (help)
  7. ^ a b Seeman P, Guan HC, Hirbec H (2009). "Dopamine D2High receptors stimulated by phencyclidines, lysergic acid diethylamide, salvinorin A, and modafinil". Synapse. 63 (8): 698–704. doi:10.1002/syn.20647. PMID 19391150. {{cite journal}}: Unknown parameter |month= ignored (help); Unknown parameter |unused_data= ignored (help)CS1 maint: multiple names: authors list (link)
  8. ^ Hirsch, JC; Crepel, F (1991). "Blockage of NMDA receptors unmasks a long-term depression in synaptic efficacy in rat profrontal neurons in vitro". Exp Brain Res. 85 (3): 621–624. PMID 1680738.
  9. ^ Breier, AK; Malhotra, DA (1997). "Association of ketamine-induced psychosis with focal activation of the prefrontal cortex in healthy volunteers". Am J Psychiatry. 154: 805–811.
  10. ^ Suzuki, Y; Jodo, E (2002). "Acute administration of phencyclidine induces tonic activation of medial prefrontal cortex neurons in freely moving rats". Neuroscience. 114 (3): 769–779.
  11. ^ Zarantonello, P; Bettini, E (2011). "Novel Analogues of ketamine and phencyclidine as NMDA receptor antagonists". Bioorganic and medicinal chemistry letters. 21 (7): 2059–2063. Retrieved July 2011. {{cite journal}}: Check date values in: |accessdate= (help)
  12. ^ Giannini AJ, Nageotte C, Loiselle RH, Malone DA, Price WA (1984). "Comparison of chlorpromazine, haloperidol and pimozide in the treatment of phencyclidine psychosis: DA-2 receptor specificity". Journal of Toxicology. Clinical Toxicology. 22 (6): 573–579. doi:10.3109/15563658408992586. PMID 6535849.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  13. ^ Castellani S, Giannini AJ, Adams PM (1982). "Effects of naloxone, metenkephalin, and morphine on phencyclidine-induced behavior in the rat". Psychopharmacology. 78 (1): 76–80. doi:10.1007/BF00470593. PMID 6815700.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ PCP synthesis and effects: table of contents
  15. ^ Itzhak Y, Kalir A, Weissman BA, Cohen S. New analgesic drugs derived from phencyclidine. Journal of Medicinal Chemistry. 1981; 24(5):496–499
  16. ^ Chaudieu I, Vignon J, Chicheportiche M, Kamenka JM, Trouiller G, Chicheportiche R. Role of the aromatic group in the inhibition of phencyclidine binding and dopamine uptake by PCP analogs. Pharmacology Biochemistry and Behaviour. 1989 Mar;32(3):699–705.
  17. ^ Olney J, Labruyere J, Price M (1989). "Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs". Science. 244 (4910): 1360–1362. doi:10.1126/science.2660263. PMID 2660263.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  18. ^ Hargreaves R, Hill R, Iversen L (1994). "Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology". Acta Neurochir Suppl (Wien). 60: 15–9. PMID 7976530.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  19. ^ Jansen, Karl. Ketamine: Dreams and Realities. MAPS, 2004. ISBN 0-9660019-7-4
  20. ^ Erowid DXM Vault : Response to "The Bad News Isn't In": Please Pass The Crow, by William E. White
  21. ^ Reynolds, Lindsay M. (March 1, 2005). "Chronic phencyclidine administration induces schizophrenia-like changes in N-acetylaspartate and N-acetylaspartylglutamate in rat brain". Schizophrenia Research. 73 (2–3): 147–152. doi:10.1016/j.schres.2004.02.003. PMID 15653257. {{cite journal}}: |access-date= requires |url= (help); Unknown parameter |coauthors= ignored (|author= suggested) (help)
  22. ^ Murray JB (2002). "Phencyclidine (PCP): a dangerous drug, but useful in schizophrenia research". J Psychol. 136 (3): 319–327. doi:10.1080/00223980209604159. PMID 12206280. {{cite journal}}: Unknown parameter |month= ignored (help)
  23. ^ Zukin, Stephen R; Sloboda, Zili; Javitt, Daniel C (2005). "Phencyclidine (PCP)". In Lowinson, Joyce H; Ruiz, Pedro; Millman, Robert B; Langrod, John G (eds.). Substance Abuse: A Comprehensive Textbook (4th ed.). Philadelphia: Lippincott Williams & Wilkins. ISBN 0-7817-3474-6. Retrieved 2 December 2010Template:Inconsistent citations {{cite book}}: External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)CS1 maint: postscript (link)
  24. ^ Inciardi 1992, p. 46.
  25. ^ Inciardi 1992, pp. 46–49.
  26. ^ Kids Use Embalming Fluid as Drug, By Joann Loviglio, July 27, ????, ABC News
  27. ^ Illegal drug users dip into embalming fluid, By Douglass Dowty, August 03, 2009, The Post-Standard
  28. ^ a b Diaz, Jaime. How Drugs Influence Behavior. Englewood Cliffs: Prentice Hall, 1996.
  29. ^ Chudler, Eric H. "Neuroscience for Kids - PCP". Neuroscience for Kids. Retrieved 2011-01-26.
  30. ^ Inciardi 1992, p. 48–49.
  31. ^ Does PCP turn people into cannibals? The Straight Dope, 2005
  32. ^ a b Inciardi 1992, p. 48.
  33. ^ Gahlinger, 2001
  34. ^ Does PCP turn people into cannibals? The Straight Dope, 2005
  35. ^ Luisada PV. The phencyclidine psychosis: phenomenology and treatment. In Petersen Rc, Stillman RC (eds). Phencyclidine (PCP) abuse: an appraisal. National Institute on Drug Abuse: Rockville, Maryland, 1978.
  36. ^ Pender JW (1972). "Dissociative anesthesia". Calif Med. 117: 46–47. PMC 1518731. PMID 18730832.
  37. ^ AJ Giannini. Drugs of Abuse—Second Edition. Los Angeles, Practice Management Information Corp.,1997,pg. 126. ISBN 1-57066-053-0.
  38. ^ a b c d Helman RS, Habal R (October 6, 2008). "Phencyclidine Toxicity". eMedicine. Retrieved on November 3, 2008.
  39. ^ a b c d Olmedo R (2002). "Chapter 69: Phencyclidine and ketamine". In Goldfrank LR, Flomenbaum NE, Lewin NA, Howland MA, Hoffman RS, Nelson LS (eds.) (ed.). Goldfrank's Toxicologic Emergencies. New York: McGraw-Hill. pp. 1034–1041. ISBN 0-07-136001-8. {{cite book}}: |editor= has generic name (help)CS1 maint: multiple names: editors list (link) Retrieved on November 3, 2008 through Google Book Search.
  40. ^ a b c Milhorn HT (1991). "Diagnosis and management of phencyclidine intoxication". American Family Physician. 43 (4): 1293–1302. PMID 2008817. {{cite journal}}: Unknown parameter |month= ignored (help)
  41. ^ Giannini AJ. Price WA. PCP: Management of acute intoxication. Medical Times. 1985;113(9):43–49
  42. ^ Giannini AJ, Eighan MS, Loiselle RH, Giannini MC (1984). "Comparison of haloperidol and chlorpromazine in the treatment of phencyclidine psychosis". Journal of Clinical Pharmacology. 24 (4): 202–204. PMID 6725621. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
Notes
  • Inciardi, James A. (1992). The War on Drugs II. Mayfield Publishing Company. ISBN 1-55934-016-9.
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