Beard was convicted of conspiracy to distribute cocaine, cocaine base, heroin and phencyclidine.
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Terence Crutcher, 40, had "acute phencyclidine intoxication" when he was shot and killed on Sept.
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The drugs for which tests are required are marijuana, cocaine, amphetamines, phencyclidine (PCP) and opiates.
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" PCP (or Phencyclidine, known on the street as "angel dust") and "drugs like that are dissociative anesthetics.
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Lamar Davenport, 33, ingested the drug phencyclidine, known as PCP, the night of the attack, in August 2015.
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Tests to detect cocaine, marijuana and phencyclidine, an illegal hallucinogenic drug also known as PCP or angel dust, added $2000,21 more.
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Inside his car they discovered a burning cigarette that contained the hallucinogenic drug phencyclidine, or P.C.P., commonly called angel dust, according to court documents.
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Different still are hallucinogens, such as lysergic acid diethylamide (LSD), or acid; mescaline and peyote; psilocybin, or "magic mushrooms"; and phencyclidine (PCP), or angel dust.
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After the shooting, the police said, officers found in the vehicle a vial of phencyclidine, known as PCP, a drug that can induce powerful hallucinations.
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The Oklahoma Medical Examiner's Office report said Crutcher had 96 nanograms per milliliter of phencyclidine, or PCP, in his bloodstream at the time of his death on Sept. 16.
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An autopsy found phencyclidine, PCP, was in Crutcher's system at the time of his fatal shooting, according to the toxicology report released with his autopsy by the Oklahoma Chief Medical Examiner's Office.
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An autopsy found Phencyclidine, or PCP, in Crutcher's system at the time of his fatal shooting, according to the toxicology report released with his autopsy by the Oklahoma Chief Medical Examiner's Office.
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Ketamine was developed more than five decades ago as a safer alternative to the anesthetic phencyclidine, or PCP, and is used worldwide, in operating rooms, on the battlefield and in pediatric clinics.
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The short history lesson behind ketamine is that it was first discovered in the 1960s and quickly put to use as a safer anesthetic alternative to phencyclidine, or PCP as it's better known.
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PCP or phencyclidine, also called angel dust, can cause slurred speech, loss of coordination and a sense of strength or invulnerability, according to the U.S. Drug Enforcement Administration and the National Institute on Drug Abuse.
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However, she also said she perceived Crutcher as reaching into his car for what she feared was a weapon, and also suspected that he was high on the hallucinogenic stimulant PCP, or phencyclidine, a suspicion born out by autopsy results.
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Ketamine, first developed in 1962 as an anesthetic, has a storied experimental past, including as a combat-zone anesthetic and party drug known as "Special K." Arguing that the effects of ketamine were similar, but less intense than phencyclidine (PCP), the Drug Enforcement Administration, in 85033, classified ketamine as a Schedule III controlled substance.
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Names like "synthetic cocaine" and "new cocaine" have been misapplied to phencyclidine (PCP) and various designer drugs.
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The late 1970s also saw the introduction of various analogues of phencyclidine (PCP) to the illicit market.
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Illicit PCP in several forms seized by the DEA. Phencyclidine is used for its ability to induce a dissociative state.
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PCPr is an arylcyclohexylamine dissociative anesthetic drug with hallucinogenic and stimulant effects. It is around the same potency as phencyclidine, although slightly less potent than its ethyl homologue eticyclidine, and has reportedly been sold as a designer drug in Germany and other European countries since the late 1990s.Christoph Sauer. Phencyclidine Derivatives – A new Class of Designer Drugs.
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Phencyclidine, the prototypal arylcyclohexylamine derivative. Arylcyclohexylamines, also known as arylcyclohexamines or arylcyclohexanamines, are a chemical class of pharmaceutical, designer, and experimental drugs.
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K. Lorch, Specificity Problem with the Cocaine- > Specific Field Test. II. Non-phenothiazine False Positives and the > Separation of Phencyclidine-promazine Combinations.
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Cyclohexanone has been used in the illicit production of phencyclidine and its analogues and as such is often subject to additional checks before purchase.
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3-Hydroxyphencyclidine (3-HO-PCP) is a dissociative of the arylcyclohexylamine class related to phencyclidine (PCP) that has been sold online as a designer drug.
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Ketamine and other arylcyclohexylamines. Other arylcyclohexylamines and analogues of ketamine include eticyclidine (PCE), 3-MeO-PCE, methoxetamine (MXE), tiletamine, phencyclidine (PCP), tenocyclidine (TCP), and many others.
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1-(1-Phenylcyclohexyl)-4-hydroxypiperidine (PCHP) is a metabolite of phencyclidine (PCP). PCHP can be detected in the hair, urine, stool, sweat, and saliva of PCP users.
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3-Methyl-PCPy is covered by drug analogue laws in various jurisdictions (UK, Germany, Japan, Australia etc) as a generic arylcyclohexylamine derivative, and a structural isomer of phencyclidine.
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Drugs of this class are unlikely candidates for pharmacological prevention of addiction because these drugs themselves are used recreationally. Examples of NMDAR antagonists are ketamine, dextromethorphan (DXM), phencyclidine (PCP).
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Some psychoactive drugs such as LSD, methaqualone, or phencyclidine (angel-dust) can cause hyperacusis. An antibiotic, ciprofloxacin, has also been seen to be a cause, known as ciprofloxacin-related hyperacusis.
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PCAA, or 5-[N-(1-phenylcyclohexyl)]-aminopentanoic acid, is a metabolite of phencyclidine (PCP). It can be detected in the urine of PCP users by mass spectrometry as means of drug screening.
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The symptoms of a hallucinogenic toxidrome include disorientation, hallucinations, hyperactive bowel sounds, panic, and seizures. Complications include hypertension, tachycardia, and tachypnea. Substances that may cause this toxidrome include substituted amphetamines, cocaine, and phencyclidine.
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Crack cocaine may be combined with amphetamine ("croack"); tobacco ("coolie"); marijuana ("buddha"; "caviar"; "chronic"; "cocoa puffs"; "fry daddy"; "gimmie"; "gremmie"; "juice"; "primo"; "torpedo"; "turbo"; "woolie"; "woola"); heroin ("moon rock"); and phencyclidine ("clicker"; "p-funk"; "spacebase").
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Phencyclidine is an NMDA receptor antagonist that blocks the activity of the NMDA receptor to cause anaesthesia and analgesia without causing cardiorespiratory depression. NMDA is an excitatory receptor in the brain, when activated normally the receptor acts as an ion channel and there is an influx of positive ions through the channel to cause nerve cell depolarisation. Phencyclidine enters the ion channel and binds, reversibly and non-competitively, inside the channel pore to block the entry of positive ions to the cell, thereby inhibiting cell depolarisation.
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Gacyclidine (GK-11) is a psychoactive drug which acts as a dissociative via functioning as a non-competitive NMDA receptor antagonist. It is closely related to phencyclidine (PCP), and specifically, is a derivative of tenocyclidine (TCP).
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Some NMDA receptor antagonists, such as ketamine, dextromethorphan (DXM), phencyclidine (PCP), methoxetamine (MXE), and nitrous oxide (N2O), are recreational drugs used for their dissociative, hallucinogenic, and euphoriant properties. When used recreationally, they are classified as dissociative drugs.
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The officers later testified that they believed King was under the influence of phencyclidine (PCP),Cannon. Official Negligence: although King's toxicology tested negative for the drug.Cannon, Lou (March 16, 1993). "Prosecution Rests Case in Rodney King Beating ".
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Intraperitoneal administration of dizocilpine also produced an enhancement in self-stimulation responding. Rhesus monkeys were trained to self-administer cocaine or phencyclidine, then were offered dizocilpine instead. None of the four monkeys who were used to cocaine chose to self-administer dizocilpine but three out of the four monkeys who had been using phencyclidine self- administered dizocilpine, suggesting again that dizocilpine has potential as a recreational drug for those seeking a dissociative anaesthetic type of experience. It was found that dizocilpine administration elicited conditioned place preference in animals, again demonstrating its reinforcing properties.
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Phencyclidine, a high-affinity ligand of PCP site 2. PCP site 2 is a binding site that was identified as a high-affinity target for phencyclidine (PCP), an anesthetic and dissociative hallucinogen that acts primarily as an NMDA receptor antagonist. The site is distinct from the PCP binding site on the NMDA receptor (otherwise known as PCP site 1) and the common/main sites on the monoamine transporters (, , ). It is associated with monoamine reuptake inhibition, and it has been suggested that the site may be an allosteric/regulatory site of the monoamine transporters.
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These investigations demonstrated ketamine's short duration of action and reduced behavioral toxicity made it a favorable choice over phencyclidine (PCP) as a dissociative anesthetic. Following FDA approval in 1970, ketamine anesthesia was first given to American soldiers during the Vietnam War.
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Dieticyclidine (PCDE), or diethylphenylcyclohexylamine, is a psychoactive drug and research chemical of the arylcyclohexylamine chemical class related to phencyclidine (PCP) and eticyclidine (PCE). It acts as an NMDA receptor antagonist but has low potency and acts mainly as a prodrug for eticyclidine.
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Dextromethorphan and its major metabolite, dextrorphan, also block the NMDA glutamate receptor at high doses, which produces effects similar to other dissociative anesthetics such as ketamine, nitrous oxide, and phencyclidine. It was patented in 1949 and approved for medical use in 1953.
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4-Phenyl-4-(1-piperidinyl)cyclohexanol, also known as PPC, is an organic chemical which is a metabolite of phencyclidine (PCP). It can be detected in the hair of PCP users. PPC has been shown to cause increases in locomotor activity in lab mice.
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Phencyclidine (PCP) is believed to be the first arylcyclohexylamine with recognized anesthetic properties, but several arylcyclohexylamines were described before PCP in the scientific literature, beginning with PCA (1-phenylcyclohexan-1-amine) the synthesis of which was first published in 1907. PCE was reported in 1953 and PCMo in 1954, with the latter compound described as a potent sedative. Arylcyclohexylamine anesthetics were intensively investigated at Parke-Davis, beginning with the 1956 synthesis of phencyclidine and later the related compound ketamine. The 1970s saw the debut of these compounds, especially PCP and its analogues, as illicitly used recreational drugs due to their dissociative hallucinogenic and euphoriant effects.
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8a-Phenyldecahydroquinoline (8A-PDHQ) is a high affinity NMDA antagonist developed by a team at Parke Davis in the 1950s.US Patent 3035059 It is a structural analog of phencyclidine with slightly lower binding affinity than the parent compound. (-)-8a-Phenyldecahydroquinoline has an in vivo potency comparable to that of (+)-MK-801.
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It may also have potential use in prevention and treatment of ischemic retinopathy and retinal and optic nerve injury. Coluracetam has been shown to reverse the loss of choline acetyltransferase production in the medial septal nucleus of rats exposed to phencyclidine (PCP), and is considered a potential therapeutic drug for schizophrenia.
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"Lack of Smooth Pursuit" is a scorable clue on the NHTSA's standardized field sobriety tests. The clue, in combination with others, may be used to determine if a person is impaired by alcohol and/or drugs. Drugs causing lack of smooth pursuit include depressants, some inhalants, and dissociative anesthetics (such as phencyclidine or ketamine).
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Several residents witnessed the shooting. Olsen said later that he had believed Hill was a threat to the officer's safety and under the influence of drugs like phencyclidine or bath salts. He told the grand jury deciding whether to indict him on charges of murder about other cases in which suspects who had used these drugs had attacked police.
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Phencyclidine or phenylcyclohexyl piperidine (PCP), also known as angel dust among other names, is a drug used for its mind-altering effects. PCP may cause hallucinations, distorted perceptions of sounds, and violent behavior. As a recreational drug, it is typically smoked, but may be taken by mouth, snorted, or injected. It may also be mixed with cannabis or tobacco.
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Both are addictive drugs, cocaine being a stimulant and phencyclidine a hallucinogen. In studying their effects on acetylcholine receptors, Hess found that both drugs inhibited the receptor and affected its equilibrium, though via different mechanisms. His findings were published in his 1982 paper “Cocaine and Phencyclidine Inhibition of the Acetylcholine Receptor: Analysis of the Mechanisms of Action Based on Measurements of Ion Flux in the Millisecond-to-Minutes Time Region.” He continued to explore different techniques for studying the acetylcholine receptor such as the one described in his paper “Acetylcholine Receptor (from Electrophorus electricus): A Comparison of Single-Channel Current Recordings and Chemical Kinetic Measurements.” He used a single-channel measurement technique to determine the currents through the channels of the acetylcholine receptor and the lifetimes of the receptor states.
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Dimethyltryptamine (DMT), 4-methyl-2,5-dimethoxyamphetamine (DOM/STP), gamma-hydroxybutyric acid (GHB), bufotenin (toad venom) and ibogaine are Schedule 1 on the California Uniform Controlled Substances Act. Phencyclidine (PCP) is Schedule 2 on the California Uniform Controlled Substances Act. PCP is illegal for possession under Health and Safety Code 11377. PCP is illegal for possession for sale under Health and Safety Code 11378.
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Diazepam is the most frequently used sedative for such treatment, but other benzodiazepines such as lorazepam are also effective. Such sedatives will only decrease fear and anxiety, but will not subdue hallucinations. In severe cases, antipsychotics such as haloperidol can reduce or stop hallucinations. Haloperidol is effective against drug- induced psychosis caused by LSD and other tryptamines, amphetamines, ketamine, and phencyclidine.
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In 1973, he received a Master of Arts from American University. While teaching, Koper continued his journalism career. His 1978 article about the emerging recreational use of the dissociative drug phencyclidine, also known as PCP, was among the early reporting on the topic, and was later cited by scholars. In 1979, he began writing for the alternative weekly Baltimore City Paper.
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Organic cation transporter 3 is a polyspecific transporter whose transport is independent of sodium. Known substrates for transport include: histamine, serotonin, norepinephrine, dopamine and MPP+. Capacity for transport and affinity for these substrates may vary between rat and human isoforms however. Transport activity of OCT3 is inhibited by recreational and pharmaceutical drugs, including MDMA, phencyclidine (PCP), MK-801, amphetamine, methamphetamine and cocaine.
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Autopsy results released by the Oklahoma State Medical Examiner indicated that Terence Crutcher had "acute phencyclidine (PCP) intoxication" at the time of the shooting. The report stated that Crutcher had 96 nanograms per milliliter of PCP in his blood at the time of death. The report also indicated that tenocyclidine (TCP), a psychostimulant and hallucinogen which is more potent than PCP, was present.
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There have been false positives reported for phencyclidine (PCP), cocaine and amphetamine with routine urine-based drug tests. Although rare these instances typically occur with higher doses of venlafaxine, more than 150 mg per day, when used for extended periods of time. In rare cases, drug-induced akathisia can occur after use in some people. Venlafaxine should be used with caution in hypertensive patients.
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Benocyclidine, also known as benzothiophenylcyclohexylpiperidine (BTCP), is a psychoactive recreational drug of the arylcyclohexylamine class which is related to phencyclidine (PCP). It was first described in a patent application naming Marc Caron and colleagues at Duke University in 1997.PCT Patent Application WO199712513 (see also US Patents Nos.5,866,756 and 6,218,595 It acts as a potent and selective dopamine reuptake inhibitor (DRI) and a psychostimulant.
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Unlike related compounds like phencyclidine and ketamine, benocyclidine is a pure DRI with negligible affinity for the NMDA receptor, and it therefore lacks any anticonvulsant, anesthetic, hallucinogenic, or dissociative effects. It has been used to label the dopamine transporter. BCP was also used to try to find a common pharmacophore for DRI type stimulants. More recently, benocyclidine has been found in several ecstasy tablets, sold as MDMA.
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Methoxetamine, abbreviated as MXE, is a dissociative hallucinogen that has been sold as a designer drug. It differs from many dissociatives such as ketamine and phencyclidine (PCP) that were developed as pharmaceutical drugs for use as general anesthetics in that it was designed for grey market distribution. MXE is an arylcyclohexylamine. It acts mainly as an NMDA receptor antagonist, similarly to other arylcyclohexylamines like ketamine and PCP.
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3-Methoxyphencyclidine (3-MeO-PCP) is a dissociative hallucinogen of the arylcyclohexylamine class related to phencyclidine (PCP) which has been sold online as a designer drug. It acts mainly as an NMDA receptor antagonist, though it has also been found to interact with the sigma σ receptor and the serotonin transporter. The drug does not possess any opioid activity nor does it act as a dopamine reuptake inhibitor.
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Ionotropic glutamate receptors can include NMDA, AMPA, and kainate receptors. These receptors are named after agonists that facilitate glutamate activity. NMDA receptors are notable for their excitatory mechanisms to affect neuronal plasticity in learning and memory, as well as neuropathologies such as stroke and epilepsy. NDMA receptors have multiple binding sites just like ionotropic GABA receptors and can be influenced by co- agonists such the glycine neurotransmitter or phencyclidine (PCP).
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Tenocyclidine (TCP) was discovered by a team at Parke-Davis in the late 1950s. Heterocyclic compounds and methods for producing the same It is a dissociative anesthetic drug with psychostimulant and hallucinogenic effects. It is similar in effects to phencyclidine (PCP) but is considerably more potent. TCP has slightly different binding properties to PCP, with more affinity for the NMDA receptors, but less affinity for the sigma receptors.
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Selfotel (CGS-19755) is a drug which acts as a competitive NMDA antagonist, directly competing with glutamate for binding to the receptor. Initial studies showed it to have anticonvulsant, anxiolytic, analgesic and neuroprotective effects, and it was originally researched for the treatment of stroke, but subsequent animal and human studies showed phencyclidine-like effects, as well as limited efficacy and evidence for possible neurotoxicity under some conditions, and so clinical development was ultimately discontinued.
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3-MeO-PCMo is a dissociative anesthetic drug which is similar in structure to phencyclidine and been sold online as a designer drug. The inhibitory effect of 3-MeO-PCMo on the reduction in the density of the drebrin clusters by NMDAR stimulation with glutamate acid is lower than that of PCP or 3-MeO-PCP, with IC50 values of 26.67 μM (3-MeO-PCMo), 2.02 μM (PCP) and 1.51 μM (3-MeO-PCP).
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Alternatively, some reuptake inhibitors bind to allosteric sites and inhibit reuptake indirectly and noncompetitively. Phencyclidine and related drugs such as benocyclidine, tenocyclidine, ketamine, and dizocilpine (MK-801), have been shown to inhibit the reuptake of the monoamine neurotransmitters. They appear to exert their reuptake inhibition by binding to vaguely characterized allosteric sites on each of the respective monoamine transporters. Benztropine, mazindol, and vanoxerine also bind to these sites and have similar properties.
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These groups reported diminished receptive ability in heroin addicts and phencyclidine abusers, contrasted with increased receptivity in cocaine addicts. Men with major depression manifested significantly decreased ability to read nonverbal cues when compared with euthymic men. In some subjects tested for ability to read nonverbal cues, intuitive paradigms were apparently employed while in others a cause and effect approach was used. Subjects in the former group answered quickly and before reinforcement occurred.
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The excitatory neurotransmitter glutamate is now also thought to be associated with schizophrenia. Phencyclidine (also known as PCP or "Angel Dust") and ketamine, both of which block glutamate (NMDA) receptors, are known to cause psychosis at least somewhat resembling schizophrenia, further suggesting that psychosis and perhaps schizophrenia cannot fully be explained in terms of dopamine function, but may also involve other neurotransmitters."Daring to Think Differently about Schizophrenia". New York Times, February 24, 2008.
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3-MeO-PCP was first synthesized in 1979 to investigate the structure–activity relationships of phencyclidine (PCP) derivatives. The effects of 3-MeO-PCP in humans were not described until 1999 when a chemist using the pseudonym John Q. Beagle wrote that 3-MeO-PCP was qualitatively similar to PCP with comparable potency. 3-MeO-PCP was preceded by the less potent dissociative 4-MeO-PCP and first became available as a research chemical in 2011.
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An Oxford Reference page defined "Beam me up, Scotty" as "a mixture of phencyclidine and cocaine" and to "talk to Scotty", "high off Scotty", "see Scotty", etc. The phrase has been referenced by Baxter County Sheriff's drug slang definitions. It is also referenced in the book "Vice Slang" by Tom Dalzell and Terry Victor, for crack cocaine, and to describe "Beamers" or "Beemers" as those taking said drugs. The exact timing of when the phrase became popular is unclear.
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Figure 4: The chemical structures of MK-801, phencyclidine and ketamine, high affinity uncompetitive NMDA receptor antagonists. Uncompetitive NMDA receptor antagonists block within the ion channel at the Mg2+ site (pore region) and prevent excessive influx of Ca2+. Noncompetitive antagonism refers to a type of block that an increased concentration of glutamate cannot overcome, and is dependent upon prior activation of the receptor by the agonist, i.e. it only enters the channel when it is opened by agonist.
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The Psychemedics technology includes tests for cocaine, marijuana, opiates (including heroin and oxycodone), methamphetamine, Ecstasy (MDMA), Eve (MDEA) and phencyclidine (PCP). A standard test of approximately one-and-one-half inches of head hair cut close to the scalp can provide a several month window to detect drug ingestion. In 2013, Psychemedics Corporation began offering hair based alcohol Ethyl glucuronide testing. This testing was previously attempted by laboratories in the United Kingdom, but has suffered from numerous lawsuits.
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A commonly held misconception is that phencyclidine (PCP, angel dust) is the same as (or is synthesized from) embalming fluid. Some people, believing this myth, have actually attempted to smoke cigarettes or cannabis dipped in real embalming fluid (i.e. formaldehyde), which is highly toxic. Conversely, some users of PCP-laced cannabis believe (and are often told) that it contains embalming fluid proper and not PCP, or that the slang term "dust" really means embalming fluid proper.
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Though the specific area of the brain responsible for latent learning may not have been pinpointed, it was found that patients with medial temporal amnesia had particular difficulty with a latent learning task which required representational processing. Another study, conducted with mice, found intriguing evidence that the absence of a prion protein disrupts latent learning and other memory functions in the water maze latent learning task. A lack of phencyclidine was also found to impair latent learning in a water finding task.
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Phencyclidine (PCP), ketamine, etoxadrol and dexoxadrol all contain phenyl and amino groups, which bind to the PCP site on the NMDA receptor. Tenocyclidine contains a thiophene ring instead, which is bioisosteric with a phenyl ring. Phenicyclidine (PCP), tenocyclidine (TCP), etoxadrol and its precursor, dexoxadrol have related chemical structures. These drugs all act similarly on the nervous system, acting as dissociative hallucinogens (meaning that they interfere with normal sensory signals, replacing them with hallucinations of any sensory modality) with anesthetic and analgesic properties.
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In animal models, NMDA antagonists increase glutamate release in the prefrontal cortex. It is postulated that this is a homeostatic response to NMDA receptor blockade, which in turn increases psychotic symptoms. A class of NMDA receptor antagonists have been denoted dissociative anesthetics because they produce a sense of depersonalization and dissociation of subjective experience from various forms of sensory input stimuli. As such, variants such as Ketamine (Angel Dust/Special K) and Phencyclidine (PCP) have become a commonly abused street-drug.
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Drugs that can trigger an oculogyric crisis include neuroleptics (such as haloperidol, chlorpromazine, fluphenazine, olanzapine), carbamazepine, chloroquine, cisplatin, diazoxide, levodopa, lithium, metoclopramide, lurasidone, domperidone, nifedipine, pemoline, phencyclidine ("PCP"), reserpine, and cetirizine, an antihistamine. High-potency neuroleptics are probably the most common cause in the clinical setting. Other causes can include Aromatic L-amino acid decarboxylase deficiency Korenke, GC; Christen, HJ; Hyland, K; Hunneman, DH; Hanefeld, F (1997). "Aromatic L-amino acid decarboxylase deficiency: an extrapyramidal movement disorder with oculogyric crises".
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Examples of antagonists, or more appropriately named receptor channel blockers, of the NMDA receptor are APV, amantadine, dextromethorphan (DXM), ketamine, magnesium, tiletamine, phencyclidine (PCP), riluzole, memantine, methoxetamine (MXE), methoxphenidine (MXP) and kynurenic acid. While dizocilpine is generally considered to be the prototypical NMDA receptor blocker and is the most common agent used in research, animal studies have demonstrated some amount of neurotoxicity, which may or may not also occur in humans. These compounds are commonly referred to as NMDA receptor antagonists.
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Sigma receptors are thought to be involved in the drug psychosis that can be induced by some drugs such as phencyclidine and cocaine, and rimcazole was originally researched as a potential antipsychotic with a different mechanism of action to traditional antipsychotic drugs. Trials proved inconclusive and rimcazole was not pursued for this application, but other sigma antagonists continue to be researched for a variety of potential applications.Volz HP, Stoll KD. Clinical trials with sigma ligands. Pharmacopsychiatry. 2004 Nov;37 Suppl 3:S214-20.
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Black market ecstasy pills are frequently found to contain other drugs in place of or in addition to methylenedioxymethylamphetamine (MDMA). Since the slang term "ecstasy" usually refers only to MDMA, any pill which contains other compounds may be considered adulterated. 3,4-Methylenedioxyamphetamine (MDA), methylenedioxyethamphetamine (MDEA), amphetamine, methylamphetamine, benzylpiperazine (BZP), trifluoromethylphenylpiperazine (TFMPP), caffeine, ephedrine, pseudoephedrine, and dextromethorphan (DXM) are all commonly found in pills being sold as ecstasy. Less common drugs in ecstasy include diphenhydramine, acetaminophen, 5-MeO-DiPT, 2C-B, procaine, and phencyclidine (PCP).
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At high doses, dextromethorphan is classified as a dissociative general anesthetic and hallucinogen, similar to the controlled substances ketamine and phencyclidine (PCP). Also like those drugs, dextromethorphan is an NMDA receptor antagonist. It generally does not produce withdrawal symptoms characteristic of physical dependence-inducing substances, but cases of psychological dependence have been reported. Due to dextromethorphan's selective serotonin reuptake inhibitor-like action, the sudden cessation of recreational dosing in tolerant individuals can result in mental and physical withdrawal symptoms similar to the withdrawal from SSRIs.
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A pile of cocaine hydrochloride A piece of compressed cocaine powder Cocaine in its purest form is a white, pearly product. Cocaine appearing in powder form is a salt, typically cocaine hydrochloride. Street cocaine is often adulterated or "cut" with talc, lactose, sucrose, glucose, mannitol, inositol, caffeine, procaine, phencyclidine, phenytoin, lignocaine, strychnine, amphetamine, or heroin. The color of "crack" cocaine depends upon several factors including the origin of the cocaine used, the method of preparation – with ammonia or baking soda – and the presence of impurities.
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Dextromethorphan gel capsules Over-the-counter preparations containing dextromethorphan have been used in manners inconsistent with their labeling, often as a recreational drug. At doses much higher than medically recommended, dextromethorphan and its major metabolite, dextrorphan, acts as an NMDA receptor antagonist, which produces dissociative hallucinogenic states somewhat similar to ketamine and phencyclidine. It may produce distortions of the visual field – feelings of dissociation, distorted bodily perception, excitement, and a loss of sense of time. Some users report stimulant-like euphoria, particularly in response to music.
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BZ was invented by the Swiss pharmaceutical company Hoffman-LaRoche in 1951. The company was investigating anti-spasmodic agents, similar to tropine, for treating gastrointestinal ailments when the chemical was discovered. It was then investigated for possible use in ulcer treatment, but was found unsuitable. At this time the United States military investigated it along with a wide range of possible nonlethal, psychoactive and psychotomimetic incapacitating agents including psychedelic drugs such as LSD and THC, dissociative drugs such as ketamine and phencyclidine, potent opioids such as fentanyl, as well as several glycolate anticholinergics.
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Ciramadol (WY-15,705) is an opioid analgesic that was developed in the late 1970s and is related to phencyclidine, tramadol, tapentadol and venlafaxine. It is a mixed agonist-antagonist for the μ-opioid receptor with relatively low abuse potential and a ceiling on respiratory depression which makes it a relatively safe drug. It has a slightly higher potency and effectiveness as an analgesic than codeine, but is weaker than morphine. Other side effects include sedation and nausea but these are generally less severe than with other similar drugs.
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Alaproclate (developmental code name GEA-654) is a drug that was being developed as an antidepressant by the Swedish pharmaceutical company Astra AB (now AstraZeneca) in the 1970s. It acts as a selective serotonin reuptake inhibitor (SSRI), and along with zimelidine and indalpine, was one of the first of its kind. Development was discontinued due to the observation of liver complications in rodent studies. In addition to its SSRI properties, alaproclate has been found to act as a non-competitive NMDA receptor antagonist, but does not have discriminative stimulus properties similar to phencyclidine.
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Rolicyclidine (PCPy) is a dissociative anesthetic drug with hallucinogenic and sedative effects. It is similar in effects to phencyclidine but is slightly less potent and has less stimulant effects instead producing a sedative effect described as being somewhat similar to a barbiturate, but with additional PCP-like dissociative, anaesthetic and hallucinogenic effects.DEA Microgram Bulletin, 8, 143, 1975 Due to its similarity in effects to PCP, PCPy was placed into the Schedule I list of illegal drugs in the 1970s, although it has never been widely abused and is now little known.
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Eticyclidine (PCE, CI-400) is a dissociative anesthetic drug with hallucinogenic effects. It is similar in effects to phencyclidine but is slightly more potent. PCE was developed by Parke-Davis in the 1970s and evaluated for anesthetic potential under the code name CI-400, but research into PCE was not continued after the development of ketamine, a similar drug with more favourable properties. 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.
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Intentionally consuming more than the recommended dosage of Delsym may result in euphoria, lack of coordination, hallucinations, apathy, feelings of dissociation, and disorientation. This is due to dextromethorphan as well as its pharmacologically-active metabolite dextrorphan, both dissociative drugs that work as NMDA receptor antagonists the same way nitrous oxide (N2O), ketamine, and phencyclidine (PCP) do. Because of the abuse potential, many pharmacies and large retail chains have begun taking precautions such as restricting sales to those under age 18 and limiting the number of sales of dextromethorphan-containing products per customer.
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During postdoctoral studies at the Australian National University with David Curtis, he helped establish the role of glutamate as a central neurotransmitter and characterised its actions between AMPA, N-Methyl-D-aspartic acid (NMDA) and kainate receptor subtypes. At the Royal Veterinary College, Lodge linked his interests in anaesthesia and glutamate receptors by making the key discovery that the dissociative anaesthetics, ketamine and phencyclidine, selectively blocked NMDA receptors. He related NMDA receptor antagonism to psychotomimetic effects. This provided a basis for the glutamate hypothesis of schizophrenia and redirected pharmaceutical search for schizophrenia therapies.
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In the early 1980s, organized international trafficking of cocaine grew. However, overproduction and tighter legal enforcement for the illegal product caused drug dealers to convert the powder to "crack" – a solid, smokable form of cocaine that could be sold in smaller quantities to more people.DoJ-DEA-History-1985-1990 This trend abated in the 1990s as increased police action coupled with a robust economy caused many potential consumers to give up or fail to take up the habit. Recent years shows an increase in the consumption of vaporized heroin, methamphetamine and Phencyclidine (PCP).
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The glycine/N-methyl-D- aspartate receptor antagonist activity is specific to the R-(+) enantiomer, whereas the sedative and ataxic effects are specific to the S-(-) enantiomer. R-(+)-HA-966 did not induce drug-appropriate responding in animals trained to discriminate phencyclidine (PCP) from saline, suggesting that the glycine receptor ligand R-(+)-HA-966 has a significantly different behavioral profile than drugs affecting the ion channel of the NMDA receptor complex. S-(−)-HA-966 has been described as a "γ-hydroxybutyric acid (GHB)-like agent" and a "potent y-butyrolactone-like sedative", but it shows no affinity for the GABAB receptor (GABABR).
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By altering receptor function in one part of the brain, abnormal activity can be induced in other parts of the brain due to the same type of receptor changes. A common example is the effect of D2 altering drugs (neuroleptics) which can help schizophrenia, but cause a variety of dyskinesias by their action on motor cortex. Modern studies are revealing details of mechanisms of damage to the nervous system such as apoptosis (programmed cell death) and free-radical disruption. Phencyclidine has been found to cause cell death in striatopallidal cells and abnormal vacuolization in hippocampal and other neurons.
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Kozikowski began his career as an organic chemist at the University of Pittsburgh. Later, following his interest in the applications of chemistry to biological problems, he joined the Mayo Clinic, and drug discovery program at the Georgetown University Medical Center. During this period his team was the first to synthesize the naturally occurring alkaloid Huperzine A, an AChE inhibitor that has memory-enhancing properties, and may be useful for the treatment of Alzheimer's disease. His team also worked on various psychotropic agents such as cocaine analogs, like Nocaine, which can potentially be used to treat stimulant addiction, and on Phencyclidine analogs to treat mental health disorders.
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The following drugs have DRI action and have been or are used clinically specifically for this property: amineptine, dexmethylphenidate, difemetorex, fencamfamine, lefetamine, levophacetoperane, medifoxamine, mesocarb, methylphenidate, nomifensine, pipradrol, prolintane, and pyrovalerone. The following drugs are or have been used clinically and possess only weak DRI action, which may or may not be clinically-relevant: adrafinil, armodafinil, bupropion, mazindol, modafinil, nefazodone, sertraline, and sibutramine. The following drugs are or have been clinically used but only coincidentally have DRI properties: benzatropine, diphenylpyraline, etybenzatropine, ketamine, nefopam, pethidine (meperidine), and tripelennamine. The following are a selection of some particularly notably abused DRIs: cocaine, ketamine, MDPV, naphyrone, and phencyclidine (PCP).
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Though less common than stimulant psychosis, stimulants such as cocaine and amphetamines as well as the dissociative drug phencyclidine (PCP, angel dust) may also cause a theorized severe and life-threatening condition known as excited delirium. This condition manifests as a combination of delirium, psychomotor agitation, anxiety, delusions, hallucinations, speech disturbances, disorientation, violent and bizarre behavior, insensitivity to pain, elevated body temperature, and hysterical strength."White Paper Report on Excited Delirium Syndrome", ACEP Excited Delirium Task Force, American College of Emergency Physicians, 10 September 2009 Despite some superficial similarities in presentation excited delirium is a distinct (and more serious) condition than stimulant psychosis. The existence of excited delirium is currently debated.
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Ketamine, a synthetic general anesthetic and one of the best-known NMDAR antagonists. Antagonists of the NMDA receptor are used as anesthetics for animals and sometimes humans, and are often used as recreational drugs due to their hallucinogenic properties, in addition to their unique effects at elevated dosages such as dissociation. When certain NMDA receptor antagonists are given to rodents in large doses, they can cause a form of brain damage called Olney's lesions. NMDA receptor antagonists that have been shown to induce Olney's lesions include ketamine, phencyclidine, and dextrorphan (a metabolite of dextromethorphan), as well as some NMDA receptor antagonists used only in research environments.
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Construction of a $5 million expansion to the hospital began in 1980. The expansion was completed in phases, with the first finishing in 1982 with the addition of three more operating rooms, totaling six, and more mechanical support equipment. The final phase was completed in 1986 which saw the addition of the other half to the fourth floor, a new dedicated intensive care unit, and the fifth floor. The fifth floor remained empty and unfinished until 2018. In August 1996, the hospital treated the cast and crew of the award-winning Titanic film after an angry crew member laced a serving of lobster chowder with the hallucinogenic drug phencyclidine (PCP).
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The activity of the NMDA receptor is affected by many psychoactive drugs such as phencyclidine (PCP), alcohol (ethanol) and dextromethorphan (DXM). The anaesthetic and analgesic effects of the drugs ketamine and nitrous oxide are partially due to their effects on NMDA receptor activity. Since 1989 memantine has been recognized to be an uncompetitive antagonist of the N-methyl-D-aspartate receptor (NMDA receptor), entering the channel of the receptor after it has been activated and thereby blocking the flow of ions. The NMDA receptor channels play an important role in synaptic plasticity and synapse formation underlying memory, learning and formation of neural networks during development in the central nervous system (CNS).
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Metaphit as a methanesulfonate salt Metaphit (1-[1-(3-Isothiocyanato)phenyl]cyclohexylpiperidine) is a research chemical that acts as an acylator of NMDARAn, sigma and DAT binding sites in the CNS. It is the m-isothiocyanate derivative of phencyclidine (PCP) and binds irreversibly (forming a covalent bond) to the PCP binding site on the NMDA receptor complex. However, later studies suggest the functionality of metaphit is mediated by sites not involved in PCP-induced passive avoidance deficit, and not related to the NMDA receptor complex. Metaphit was also shown to prevent d-amphetamine induced hyperactivity, while significantly depleting dopamine content in the nucleus accumbens.
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Ketamine, a fast-acting general anesthetic derived from phencyclidine and use as a pediatric inductor, plays a non-well known role in the neural network dynamics at the healthy brain . The administration of ketamine in abnormal brain has the potential of reduce the increased function of the networks that are seen in depression. The therapeutic potential of ketamine may be explained by reversing disturbances in the glutamatergic system and restoring parts of a disrupted neurobehavioral homeostasis where several structural, metabolic, and functional abnormalities have taken place. Long term ketamine treatments lead to cognitive impairment including problems of short-term memory, visual and verbal memory.
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Licostinel (INN) (code name ACEA-1021) is a competitive, silent antagonist of the glycine site of the NMDA receptor (Kb = 5 nM). It was under investigation by Acea Pharmaceuticals as a neuroprotective agent for the treatment of cerebral ischemia associated with stroke and head injuries but was ultimately never marketed. In clinical trials, licostinel did not produce phencyclidine- like psychotomimetic effects at the doses tested, though transient sedation, dizziness, and nausea were observed. In addition to its actions at the NMDA receptor, licostinel also acts as an antagonist of the AMPA and kainate receptors at high concentrations (Kb = 0.9 μM and 2.5 μM, respectively).
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The pain stimulus can be manual, using a pain compliance hold or can be through the use of weapons such as an electroshock weapon (Taser) or ballistic round. Pain compliance as part of an escalation of force policy normally presumes a rational adversary, but some altered states such as mental illness, phencyclidine and amphetamine use, or extreme adrenaline may alter the subject's perception of pain or willingness to submit. Like other forms of non-lethal force, such pain compliance strategies are not perfect and may be abused as a form of torture, with plausible deniability. For this reason the use of pain compliance is often subject to explicit rules of engagement designed to prevent abuse and avoid conflict escalation.
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The drug phencyclidine (more commonly known as PCP) antagonizes glutamic acid non-competitively at the NMDA receptor. For the same reasons, dextromethorphan and ketamine also have strong dissociative and hallucinogenic effects. Acute infusion of the drug LY354740 (also known as eglumegad, an agonist of the metabotropic glutamate receptors 2 and 3) resulted in a marked diminution of yohimbine-induced stress response in bonnet macaques (Macaca radiata); chronic oral administration of LY354740 in those animals led to markedly reduced baseline cortisol levels (approximately 50 percent) in comparison to untreated control subjects. LY354740 has also been demonstrated to act on the metabotropic glutamate receptor 3 (GRM3) of human adrenocortical cells, downregulating aldosterone synthase, CYP11B1, and the production of adrenal steroids (i.e.
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Also, the effect can be non-specific, with head twitch responses also produced by some drugs that do not act through 5-HT2 receptors, such as phencyclidine, yohimbine, atropine and cannabinoid receptor antagonists. As well, compounds such as 5-HTP, fenfluramine and 1-Methylpsilocin can also produce head twitch and do stimulate serotonin receptors, but are not hallucinogenic in humans. This means that while the head twitch response can be a useful indicator as to whether a compound is likely to display hallucinogenic activity in humans, the induction of a head twitch response does not necessarily mean that a compound will be hallucinogenic, and caution should be exercised when interpreting such results.
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Users tend to report that the experience is not as enjoyable as other dissociative drugs, and it is often accompanied by strong auditory hallucinations. Also, dizocilpine is much longer-lasting than similar dissociative drugs such as ketamine and phencyclidine (PCP), and causes far worse amnesia and residual deficits in thinking, which have hindered its acceptance as a recreational drug. Several animal studies have demonstrated the addictive potential of dizocilpine. Rats learned to lever-press in order to obtain injections of dizocilpine into the nucleus accumbens and frontal cortex, however, when given a dopamine antagonist at the same time, the lever-pressing was not altered, which shows that the rewarding effect of dizocilpine is not dependent on dopamine.
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Various psychoactive substances (both legal and illegal) have been implicated in causing, exacerbating, or precipitating psychotic states or disorders in users, with varying levels of evidence. This may be upon intoxication for a more prolonged period after use, or upon withdrawal. Individuals who have a substance induced psychosis tend to have a greater awareness of their psychosis and tend to have higher levels of suicidal thinking compared to individuals who have a primary psychotic illness. Drugs commonly alleged to induce psychotic symptoms include alcohol, cannabis, cocaine, amphetamines, cathinones, psychedelic drugs (such as LSD and psilocybin), κ-opioid receptor agonists (such as enadoline and salvinorin A) and NMDA receptor antagonists (such as phencyclidine and ketamine).
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Beside the dopamine hypothesis, interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in the pathophysiology of schizophrenia. This has largely been suggested by lower levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia and the discovery that glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition. The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in schizophrenia. Positive symptoms fail however to respond to glutamatergic medication.
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He looked at the way that these concentrations affected the active and inactive states of the channel, and determined that the equilibrium position of this channel was one-fourth of the way open. In his 1981 articles “Acetylcholine-Induced Cation Translocation Across Cell Membranes and Inactivation of the Acetylcholine Receptor: Chemical Kinetic Measurements in the Millisecond Time Region” and “Comparison of Acetylcholine Receptor- Controlled Cation Flux in Membrane Vesicles from Torpedo californica and Electrophorus electricus: Chemical Kinetic Measurements in the Millisecond Region,” Hess discussed his findings on the rate and equilibrium changes of the acetylcholine receptor in the active versus inactive states. He conducted this study using the novel quench flow technique which allowed measurements down to the 2-millisecond interval. Using this quench flow technique, Hess then investigated the effects of cocaine and phencyclidine (commonly known as PCP) on the flux of the acetylcholine receptor.
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Histrionicotoxin has been shown to bind competitively with many local anesthetics, such as tetracaine, as well as other aromatic amine non-competitive antagonists of the receptors, indicating the compounds likely share a binding site; this site of interaction is located outside the transmembrane domain of the nicotinic acetylcholine receptor, though the exact interaction remains uncharacterized. While histrionicotoxin does share a binding location with other non-competitive antagonists of the nicotinic acetylcholine receptor, it has been proven to have relatively higher affinity for desensitized receptors than phencyclidine, indicating further yet uncharacterized subtlety in the nature of its binding. Additionally, studies of the effects of histrionicotoxin on end-plate potential have shown that the compound hinders membrane potential propagation, but has emergent characteristics with membrane hyperpolarizations. The binding of histrionicotoxin is rapidly reversible, and so it can be readily removed from affected regions with repeated washing, or, in vivo, with natural bodily diffusion.
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His research on acetylcholine receptors spanned the length of his whole career. He studied the mechanisms of these receptors, their response to flux, cocaine, phencyclidine, other inhibitors, and their changes in rate and equilibrium. In his 1976 publication “Functional Acetylcholine Receptor-Electroplax Membrane Microsacs (Vesicles): Purification and Characterization,” Hess determines the utilization of functional versus nonfunctional microsacs and how they account for the efficiency differences in muscle and nerve cells. In his paper “Acetylcholine-Receptor-Mediated Ion Flux in Electroplax Membrane Microsacs (Vesicles): Change in Mechanism Produced by Asymmetrical Distribution of Sodium and Potassium Ions,” published two years later, Hess explored the biphasic flux and desensitization of the acetylcholine receptor in connection with microsac function. He continued studying the relationship between the acetylcholine receptor and flux in his article published in 1980: “Molecular Mechanism of Acetylcholine Receptor- Controlled Ion Translocation Across Cell Membranes.” He studied these channels in the cells of the electric organs of the Electrophorus electricus and the Torpedo californica.
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Eglumegad and related drugs are neuroprotective and are synergistic with the neuroprotection produced by N-methyl-D-aspartic acid (NMDA) antagonist drugs, which may make these drugs useful in aiding recovery from brain injury. This class of drugs also interacts with hallucinogenic drugs, with eglumegad reducing the effects of 5HT2A agonist hallucinogens, while conversely the mGluR2/3 antagonist LY341495 increased the behavioural effects of these drugs. This suggests that mGluR2/3 agonists such as eglumegad may have potential uses in the treatment of some forms of psychosis, although eglumegad had only limited effects on the action of the dissociative drug phencyclidine which is generally a better model for schizophrenia than the 5HT2A agonist hallucinogens. Eglumegad also interferes in the hypothalamic–pituitary–adrenal axis, with chronic oral administration of this drug leading to markedly reduced baseline cortisol levels in bonnet macaques (Macaca radiata); acute infusion of eglumegad resulted in a marked diminution of yohimbine-induced stress response in those animals.
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Several antipsychotics are also antagonists at the 5-HT2C receptor, leading to dopamine release in the structures where 5-HT2C is expressed; striatum, prefrontal cortex, nucleus accumbens, amygdala, hippocampus (all structures indicated in this disease), and currently thought to be a reason why antipsychotics with 5HT2C antagonistic properties improves negative symptoms. More research is needed to explain the exact nature of the altered chemical transmission in this disorder. Recent evidence on a variety of animal models of psychosis, such as sensitization of animal behaviour by amphetamine, or phencyclidine (PCP, Angel Dust), or excess steroids, or by removing various genes (COMT, DBH, GPRK6, RGS9, RIIbeta), or making brain lesions in newborn animals, or delivering animals abnormally by Caesarian section, all induce a marked behavioural supersensitivity to dopamine and a marked rise in the number of dopamine D2 receptors in the high-affinity state for dopamine. This latter work implies that there are multiple genes and neuronal pathways that can lead to psychosis and that all these multiple psychosis pathways converge via the high-affinity state of the D2 receptor, the common target for all antipsychotics, typical or atypical.
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Substance use disorder (SUD) is the persistent use of drugs (including alcohol) despite substantial harm and adverse consequences. Substance use disorders are characterized by an array of mental/emotional, physical, and behavioral problems such as chronic guilt; an inability to reduce or stop consuming the substance(s) despite repeated attempts; driving while intoxicated; and physiological withdrawal symptoms. Drug classes that are involved in SUD include: alcohol; caffeine; cannabis; phencyclidine and other hallucinogens, such as arylcyclohexylamines; inhalants; opioids; sedatives, hypnotics, or anxiolytics; stimulants; tobacco; and other or unknown substances. In the Diagnostic and Statistical Manual of Mental Disorders 5th edition (2013), also known as DSM-5, the DSM-IV diagnoses of substance abuse and substance dependence were merged into the category of substance use disorders. The severity of substance use disorders can vary widely; in the DSM-5 diagnosis of a SUD, the severity of an individual's SUD is qualified as mild, moderate, or severe on the basis of how many of the 11 diagnostic criteria are met. The International Classification of Diseases 11th revision (ICD-11) divides substance use disorders into two categories: (1) harmful pattern of substance use; and (2) substance dependence.
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Avpr1a transcripts are diurnally expressed 12 hours out of phase from vasopressin expression in vasopressin and vasoactive intestinal polypeptide neurons of the suprachiasmatic nucleus in both vasopressin-normal Sprague-Dawley rats, as well as vasopressin-deficient Brattleboro rats. Rats with reduced Avpr1a in the bed nucleus of the stria terminalis have increased incidences of the isolation potentiated startle, a measure of isolation-induced anxiety. Subchronic phencyclidine (PCP) treatment (which induces symptoms similar to those of schizophrenia) reduces Avpr1a density in many brain regions, implying there might be a role for AVPR1A in schizophrenia. Avpr1a is present in the lateral septum, neocortical layer IV, hippocampal formation, amygdalostriatal area, bed nucleus of the stria terminalis, suprachiasmatic nucleus, ventral tegmental area, substantia nigra, superior colliculus, dorsal raphe, nucleus of the solitary tract, spinal cord, and inferior olive, while mRNA transcripts for Avpr1a are found in the olfactory bulb, hippocampal formation, lateral septum, suprachiasmatic nucleus, paraventricular nucleus, anterior hypothalamic area, arcuate nucleus, lateral habenula, ventral tegmental area, substantia nigra (pars compacta), superior colliculus, raphe nuclei, locus coeruleus, inferior olive, choroid plexus, endothelial cells, area postrema and nucleus of the solitary tract.
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