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Hi Liam PCP is well known for its primary action on [[ionotropic]] [[glutamate receptors]], such as the [[NMDA receptor]] in rats and in rat brain homogenate.<ref>{{cite journal |last1=Large |first1=CH |last2=Bison |first2=S |year=2011 |title=The Efficacy of Sodium Channel Blockers to Prevent Phencyclidine-Induced Cognitive Dysfunction in the Rat: Potential for Novel Treatments for Schizophrenia |journal=Journal of pharmacology and experimental therapeutics |volume=338 |issue=1 |pages=100–113 = |doi= 10.1124/jpet.110.178475|url=http://jpet.aspetjournals.org/content/338/1/100.abstract |accessdate=July 2011 |last3=Sartori |first3=I. |last4=Read |first4=K. D. |last5=Gozzi |first5=A. |last6=Quarta |first6=D. |last7=Antolini |first7=M. |last8=Hollands |first8=E. |last9=Gill |first9=C. H. |last10=Gunthorpe |first10=M. J. |last11=Idris |first11=N. |last12=Neill |first12=J. C. |last13=Alvaro |first13=G. S. }}</ref><ref name="pmid19391150">{{cite journal | author = Seeman P, Guan HC, Hirbec H | title = Dopamine D2High receptors stimulated by phencyclidines, lysergic acid diethylamide, salvinorin A, and modafinil | journal = Synapse | volume = 63 | issue = 8 | pages = 698–704 |date=August 2009 | pmid = 19391150 | doi = 10.1002/syn.20647}}</ref> As such, PCP is an NMDA receptor antagonist. The role of NMDAR antagonism in the effect of PCP, ketamine and related dissociative agents was first published by the early 1980s by David Lodge and colleagues.<ref name="Morris"/> Other NMDA receptor antagonists include [[ketamine]],<ref name=Caddy2010>Caddy C et al. Ketamine as the prototype glutamatergic antidepressant: pharmacodynamic actions, and a systematic review and meta-analysis of efficacy. Ther Adv Psychopharmacol. 2014 Apr;4(2):75-99. doi: 10.1177/2045125313507739. Review. PMID 24688759 PMC 3952483</ref> [[tiletamine]],<ref>{{cite journal|last=Klockgether|first=Thomas|coauthors=Turski, Lechoslaw, Schwarz, Michael, Sontag, Karl-Heinz, Lehmann, John|title=Paradoxical convulsant action of a novel non-competitiveN-methyl-d-aspartate (NMDA) antagonist, tiletamine|journal=Brain Research|date=1 October 1988|volume=461|issue=2|pages=343–348|doi=10.1016/0006-8993(88)90265-X|pmid=2846121}}</ref> [[dextromethorphan]],<ref name=Burns>Burns JM, Boyer EW. Antitussives and substance abuse. Subst Abuse Rehabil. 2013 Nov 6;4:75-82. doi: 10.2147/SAR.S36761. eCollection 2013. PMID 24648790 PMCID PMC3931656</ref> [[nitrous oxide]], [[MK-801]], and [[dexoxadrol]].
PCP is well known for its primary action on [[ionotropic]] [[glutamate receptors]], such as the [[NMDA receptor]] in rats and in rat brain homogenate.<ref>{{cite journal |last1=Large |first1=CH |last2=Bison |first2=S |year=2011 |title=The Efficacy of Sodium Channel Blockers to Prevent Phencyclidine-Induced Cognitive Dysfunction in the Rat: Potential for Novel Treatments for Schizophrenia |journal=Journal of pharmacology and experimental therapeutics |volume=338 |issue=1 |pages=100–113 = |doi= 10.1124/jpet.110.178475|url=http://jpet.aspetjournals.org/content/338/1/100.abstract |accessdate=July 2011 |last3=Sartori |first3=I. |last4=Read |first4=K. D. |last5=Gozzi |first5=A. |last6=Quarta |first6=D. |last7=Antolini |first7=M. |last8=Hollands |first8=E. |last9=Gill |first9=C. H. |last10=Gunthorpe |first10=M. J. |last11=Idris |first11=N. |last12=Neill |first12=J. C. |last13=Alvaro |first13=G. S. }}</ref><ref name="pmid19391150">{{cite journal | author = Seeman P, Guan HC, Hirbec H | title = Dopamine D2High receptors stimulated by phencyclidines, lysergic acid diethylamide, salvinorin A, and modafinil | journal = Synapse | volume = 63 | issue = 8 | pages = 698–704 |date=August 2009 | pmid = 19391150 | doi = 10.1002/syn.20647}}</ref> As such, PCP is an NMDA receptor antagonist. The role of NMDAR antagonism in the effect of PCP, ketamine and related dissociative agents was first published by the early 1980s by David Lodge and colleagues.<ref name="Morris"/> Other NMDA receptor antagonists include [[ketamine]],<ref name=Caddy2010>Caddy C et al. Ketamine as the prototype glutamatergic antidepressant: pharmacodynamic actions, and a systematic review and meta-analysis of efficacy. Ther Adv Psychopharmacol. 2014 Apr;4(2):75-99. doi: 10.1177/2045125313507739. Review. PMID 24688759 PMC 3952483</ref> [[tiletamine]],<ref>{{cite journal|last=Klockgether|first=Thomas|coauthors=Turski, Lechoslaw, Schwarz, Michael, Sontag, Karl-Heinz, Lehmann, John|title=Paradoxical convulsant action of a novel non-competitiveN-methyl-d-aspartate (NMDA) antagonist, tiletamine|journal=Brain Research|date=1 October 1988|volume=461|issue=2|pages=343–348|doi=10.1016/0006-8993(88)90265-X|pmid=2846121}}</ref> [[dextromethorphan]],<ref name=Burns>Burns JM, Boyer EW. Antitussives and substance abuse. Subst Abuse Rehabil. 2013 Nov 6;4:75-82. doi: 10.2147/SAR.S36761. eCollection 2013. PMID 24648790 PMCID PMC3931656</ref> [[nitrous oxide]], [[MK-801]], and [[dexoxadrol]].


NMDA receptors are excitatory ionotropic rceptors,<ref>{{cite journal |last1=Hirsch |first1=JC |last2=Crepel |first2=F |year=1991 |title=Blockage of NMDA receptors unmasks a long-term depression in synaptic efficacy in rat profrontal neurons in vitro |journal=Exp Brain Res |volume=85 |issue=3 |pages=621–624 |doi= 10.1007/BF00231747|pmid = 1680738 }}</ref> however, studies have shown that PCP unexpectedly produces substantial cortical activation in humans<ref>{{cite journal |last1=Breier |first1=AK |last2=Malhotra |first2=DA |year=1997 |title=Association of ketamine-induced psychosis with focal activation of the prefrontal cortex in healthy volunteers |journal=Am J Psychiatry |volume=154 |pages=805–811 |pmid=9167508 |last3=Pinals |first3=DA |last4=Weisenfeld |first4=NI |last5=Pickar |first5=D |issue=6 |doi=10.1176/ajp.154.6.805}}</ref> and rodents.<ref>{{cite journal |last1=Suzuki |first1=Y |last2=Jodo |first2=E |year=2002 |title=Acute administration of phencyclidine induces tonic activation of medial prefrontal cortex neurons in freely moving rats |journal=Neuroscience |volume=114 |issue=3 |pages=769–779 |doi=10.1016/S0306-4522(02)00298-1 |pmid=12220577 |last3=Takeuchi |first3=S |last4=Niwa |first4=S |last5=Kayama |first5=Y }}</ref>
NMDA receptors are excitatory ionotropic rceptors,<ref>{{cite journal |last1=Hirsch |first1=JC |last2=Crepel |first2=F |year=1991 |title=Blockage of NMDA receptors unmasks a long-term depression in synaptic efficacy in rat profrontal neurons in vitro |journal=Exp Brain Res |volume=85 |issue=3 |pages=621–624 |doi= 10.1007/BF00231747|pmid = 1680738 }}</ref> however, studies have shown that PCP unexpectedly produces substantial cortical activation in humans<ref>{{cite journal |last1=Breier |first1=AK |last2=Malhotra |first2=DA |year=1997 |title=Association of ketamine-induced psychosis with focal activation of the prefrontal cortex in healthy volunteers |journal=Am J Psychiatry |volume=154 |pages=805–811 |pmid=9167508 |last3=Pinals |first3=DA |last4=Weisenfeld |first4=NI |last5=Pickar |first5=D |issue=6 |doi=10.1176/ajp.154.6.805}}</ref> and rodents.<ref>{{cite journal |last1=Suzuki |first1=Y |last2=Jodo |first2=E |year=2002 |title=Acute administration of phencyclidine induces tonic activation of medial prefrontal cortex neurons in freely moving rats |journal=Neuroscience |volume=114 |issue=3 |pages=769–779 |doi=10.1016/S0306-4522(02)00298-1 |pmid=12220577 |last3=Takeuchi |first3=S |last4=Niwa |first4=S |last5=Kayama |first5=Y }}</ref>

Revision as of 14:24, 15 April 2015

For the industrial chemical also known as PCP, used as a pesticide and a disinfectant, see Pentachlorophenol.
Phencyclidine
Clinical data
AHFS/Drugs.comphencyclidine
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
ChEBI
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)
  • C1(C2(N3CCCCC3)CCCCC2)=CC=CC=C1
  • 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)
 ☒NcheckY (what is this?)  (verify)

Phencyclidine (a complex clip of the chemical name 1-(1-phenylcyclohexyl)piperidine), commonly initialized as PCP and known colloquially as Angel Dust and by many other names,[1] is a dissociative drug. PCP was brought to market in the 1950s as an anesthetic pharmaceutical drug but was soon taken off the market in 1965 due to the high prevalence of dissociative hallucinogenic side effects. 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.[2]

In chemical structure, PCP is a member of the arylcyclohexylamine class, and, in pharmacology, it is a member of the family of dissociative anesthetics. PCP works primarily as an NMDA receptor antagonist, where it blocks the activity of the NMDA receptor. Like most hallucinogenic drugs, there is risk of abuse with PCP.[3][4] In the 1970s, the US media demonized PCP and PCP users giving many outlandish claims including that PCP gave users superhuman strength.[2]

As a recreational drug, PCP may be ingested orally, smoked, insufflated or injected.[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 receptor antagonist. The role of NMDAR antagonism in the effect of PCP, ketamine and related dissociative agents was first published by the early 1980s by David Lodge and colleagues.[2] Other NMDA receptor antagonists include ketamine,[8] tiletamine,[9] dextromethorphan,[10]  nitrous oxide, MK-801, and dexoxadrol.

NMDA receptors are excitatory ionotropic rceptors,[11] however, studies have shown that PCP unexpectedly produces substantial cortical activation in humans[12] and rodents.[13] Research also indicates that PCP inhibits nicotinic acetylcholine (nACh) receptors among other mechanisms. Analogues of PCP exhibit varying potency at nACh receptors[14] and NMDA receptors.[15] Findings demonstrate that presynaptic nicotinic acetylcholine (nACh) and NMDA receptor interactions influence postsynaptic maturation of glutamatergic synapses and consequently impact synaptic development and plasticity in the brain.[16] These effects can lead to inhibition of excitatory glutamate activity in certain brain regions such as the hippocampus[17] and cerebellum[18] thus potentially leading to memory loss as one of the effects of prolonged use. Acute effects on the cerebellum manifest as changes in blood pressure, breathing rate, pulse rate, and loss of muscular coordination during intoxication.[19]

PCP, like ketamine, also acts as a D2 receptor partial agonist in rat brain homogenate[7] and has affinity for human cloned D2 receptors.[20] This activity may be associated with some of the other 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.[21]

In addition to its well explored interactions with NMDA receptors, PCP has also been to shown to associate with certain dopamine reuptake carrier proteins, and thereby lead to increased levels of available dopamine.[22]

Additionally, studies on rats indicate that PCP indirectly interacts with endorphin and enkephalin receptors to produce analgesia.[23]

Pharmacokinetics

PCP is metabolized into PCHP, PPC and PCAA.

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

Conversion of PCP into PC and piperidine by heat.

Structural analogues

Possible Analogues of PCP

Fewer than 30 different analogues of PCP were reported as being used on the street during the 1970s and 1980s, mainly in the USA.[2] The best known of these are rolicyclidine (PCPy or 1-(1-phenylcyclohexyl)pyrrolidine); eticyclidine (PCE or N-ethyl-1-phenylcyclohexylamine); and tenocyclidine (TCP or 1-(1-(2-thienyl)cyclohexyl)piperidine).[24] Only of a few of these compounds were widely used.[2]

The generalized structural motif required for PCP-like activity is derived from structure-activity relationship studies of PCP derivatives, and summarized in the illustration (left). All of these derivatives are likely to share some of their psychoactive effects with PCP itself, although a range of potencies and varying mixtures of anesthetic, dissociative and stimulant effects are known, depending on the particular drug and its substituents. 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 if sold for human consumption, even though many of them have never been made or tested.[25][26][clarification needed]

Brain effects

Some studies found that, like other NMDA receptor antagonists, phencyclidine can cause a kind of brain damage called Olney's lesions in rats.[27][28] 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,[29] but due to the study never having been published, its validity is controversial.

Phencyclidine 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.[30] It also induces symptoms in humans that mimic schizophrenia.[31]

History and medicinal use

It is commonly mistakenly reported that PCP was first synthesized in 1926.[32] This early synthesis, in fact, refers to the PCP intermediate PCC.[2] PCP was actually discovered serendipitously by Victor Maddox, a chemist at Parke-Davis in Michigan, while investigating synthetic analgesic agents. Although unexpected, PCP was identified as potentially interesting, and as such, was submitted for pharmacological testing. The promising results of these pharmacological investigations led to the rapid development of PCP. It was approved for use as an investigational drug under the tradename named Sernyl in the 1950s as an anesthetic, but because of its long half-life and adverse side effects, such as hallucinations, mania, delirium, and disorientation, it was removed from the market in 1965 and limited to veterinary use.[2][33][34]

Recreational uses

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.[35]: 46  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.[35]: 46–49 

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, tobacco, parsley, or ginger leaves, then smoked.[citation needed]

PCP is a Schedule II substance in the United States and its ACSCN is 7471.[36] Its manufacturing quota for 2014 was 19 grams.[37]

It is a Schedule I drug by the Controlled Drugs and Substances act in Canada, a List I drug of the Opium Law in the Netherlands, and a Class A substance in the United Kingdom.[citation needed]

Methods of administration

In its pure (free base) form, PCP is a solid with a low melting point (46 degrees Celsius). It is often found as a yellow oil (usually dissolved in petroleum ether, 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 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.[38][39] 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" (shermingham), "D-Bone" "leak", "Dust", "amp", "lovely", "toe tag", "dipper", "T-Bone", "happy stick", "greeners", "clicker", or "wet stick".

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.[40] Users frequently 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.[41]

Psychological effects include severe changes in body image, loss of ego boundaries, paranoia, and depersonalization. Hallucinations, euphoria, and suicidal impulses are also reported, as well as occasional aggressive behavior.[35]: 48–49 [40] Like many other drugs, phencyclidine has been known to alter mood states in an unpredictable fashion, causing some individuals to become detached, and others to become animated. PCP may induce feelings of strength, power, and invulnerability as well as a numbing effect on the mind.[5]

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 are unusual and often limited to individuals with reputations for aggression regardless of drug use.[35]: 48  This said, there have been a few, very-televised events of PCP-intoxicated individuals acting in an unpredictable fashion, possibly driven by their delusions or hallucinations. One famous example is the case of Big Lurch, a former rapper with a history of violent crime, who was convicted of murdering and cannibalizing his roommate while under the influence of PCP.[42] Other commonly cited types of incidents include inflicting property damage and self-mutilation of various types, such as pulling one's own teeth.[35]: 48 [42] These effects were not noted in its medicinal use in the 1950s and 1960s, however, and reports of physical violence on phencyclidine have often been shown to be unfounded.[43][44]

Recreational doses of the drug also occasionally appear to induce a psychotic state that resembles a schizophrenic episode, sometimes lasting for months at a time.[45] Users generally report feeling detached from reality.[46]

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.[47]

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.[48][49][50] 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.[48][49] If an antipsychotic is given, intramuscular haloperidol has been recommended.[50][51][52]

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.[48][49][50] 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.[48][49]

See also

References

  1. ^ US Department of Justice, National Drug Intelligence Center. PCP Fast Facts
  2. ^ a b c d e f g 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: 614–632. doi:10.1002/dta.1620. {{cite journal}}: Cite has empty unknown parameter: |1= (help)
  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; Sartori, I.; Read, K. D.; Gozzi, A.; Quarta, D.; Antolini, M.; Hollands, E.; Gill, C. H.; Gunthorpe, M. J.; Idris, N.; Neill, J. C.; Alvaro, G. 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 =. doi:10.1124/jpet.110.178475. Retrieved July 2011. {{cite journal}}: Check date values in: |accessdate= (help)
  7. ^ a b Seeman P, Guan HC, Hirbec H (August 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}}: CS1 maint: multiple names: authors list (link)
  8. ^ Caddy C et al. Ketamine as the prototype glutamatergic antidepressant: pharmacodynamic actions, and a systematic review and meta-analysis of efficacy. Ther Adv Psychopharmacol. 2014 Apr;4(2):75-99. doi: 10.1177/2045125313507739. Review. PMID 24688759 PMC 3952483
  9. ^ Klockgether, Thomas (1 October 1988). "Paradoxical convulsant action of a novel non-competitiveN-methyl-d-aspartate (NMDA) antagonist, tiletamine". Brain Research. 461 (2): 343–348. doi:10.1016/0006-8993(88)90265-X. PMID 2846121. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  10. ^ Burns JM, Boyer EW. Antitussives and substance abuse. Subst Abuse Rehabil. 2013 Nov 6;4:75-82. doi: 10.2147/SAR.S36761. eCollection 2013. PMID 24648790 PMCID PMC3931656
  11. ^ 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. doi:10.1007/BF00231747. PMID 1680738.
  12. ^ Breier, AK; Malhotra, DA; Pinals, DA; Weisenfeld, NI; Pickar, D (1997). "Association of ketamine-induced psychosis with focal activation of the prefrontal cortex in healthy volunteers". Am J Psychiatry. 154 (6): 805–811. doi:10.1176/ajp.154.6.805. PMID 9167508.
  13. ^ Suzuki, Y; Jodo, E; Takeuchi, S; Niwa, S; Kayama, Y (2002). "Acute administration of phencyclidine induces tonic activation of medial prefrontal cortex neurons in freely moving rats". Neuroscience. 114 (3): 769–779. doi:10.1016/S0306-4522(02)00298-1. PMID 12220577.
  14. ^ Aguayo, LG; Warnick, JE; Maayani, S; Glick, SD; Weinstein, H; Albuquerque, EX (1982). "Site of action of phencyclidine. IV. Interaction of phencyclidine and its analogues on ionic channels of the electrically excitable membrane and nicotinic receptor: implications for behavioral effects". Molecular Pharmacology. 21 (3): 637–647. PMID 6287200.
  15. ^ Zarantonello, P; Bettini, E; Paio, A; Simoncelli, C; Terreni, S; Cardullo, F (2011). "Novel Analogues of ketamine and phencyclidine as NMDA receptor antagonists". Bioorganic and medicinal chemistry letters. 21 (7): 2059–2063. doi:10.1016/j.bmcl.2011.02.009. PMID 21334205. Retrieved July 2011. {{cite journal}}: Check date values in: |accessdate= (help)
  16. ^ Lin, H; Vicini, S; Hsu, FC; Doshi, S; Takano, H; Coulter, DA; Lynch, DR (2010). "Axonal α7 nicotinic ACh receptors modulate presynaptic NMDA receptor expression and structural plasticity of glutamatergic presynaptic boutons". Proc Natl Acad Sci USA. 107 (38): 16661–16666. doi:10.1073/pnas.1007397107. PMC 2944730. PMID 20817852.
  17. ^ Fisher, JL; Dani, JA (2000). "Nicotinic receptors on hippocampal cultures can increase synaptic glutamate currents while decreasing the NMDA-receptor component". Neuropharmacology. 39 (13): 2756–69. doi:10.1016/s0028-3908(00)00102-7. PMID 11044745.
  18. ^ Prestori, F; Bonardi, C; Mapelli, L; Lombardo, P; Goselink, R; De Stefano, ME; Gandolfi, D; Mapelli, J; Bertrand, D; Schonewille, M; De Zeeuw, C; D'Angelo, E (2013). "Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stage". PLOS ONE. 8 (5): e64828. doi:10.1371/journal.pone.0064828. PMC 3669396. PMID 23741401.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  19. ^ National Institute on Drug Abuse
  20. ^ Seeman, P; Ko F and Tallerico, T (April 2005). "Dopamine receptor contribution to the action of PCP, LSD and ketamine psychotomimetics". Molecular Psychiatry. 10 (9): 877–883. doi:10.1038/sj.mp.4001682. PMID 15852061.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  21. ^ 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)
  22. ^ Rothman RB, Reid AA, Monn JA, Jacobson AE, Rice KC |year=1989 |title=The psychotomimetic drug phencyclidine labels two high affinity binding sites in guinea pig brain: evidence for N-methyl-D-aspartate-coupled and dopamine reuptake carrier-associated phencyclidine binding sites |journal=Molecular Pharmacology |volume=36 |issue=6 |pages=887-96
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