Excitatory Amino Acid Antagonists
Substance Abuse Detection
Dose-Response Relationship, Drug
Effects of stimulants of abuse on extrapyramidal and limbic neuropeptide Y systems. (1/421)Neuropeptide Y (NPY), an apparent neuromodulating neuropeptide, has been linked to dopamine systems and dopamine-related psychotic disorders. Because of this association, we determined and compared the effects of psychotomimetic drugs on extrapyramidal and limbic NPY systems. We observed that phencyclidine, methamphetamine (METH), (+)methylenedioxymethamphetamine (MDMA), and cocaine, but not (-)MDMA, similarly reduced the striatal content of NPY-like immunoreactivity from 54% (phencyclidine) to 74% [(+) MDMA] of control. The effects of METH on NPY levels in the nucleus accumbens, caudate nucleus, globus pallidus, and substantia nigra were characterized in greater detail. We observed that METH decreased NPY levels in specific regions of the nucleus accumbens and the caudate, but had no effect on NPY in the globus pallidus or the substantia nigra. The dopamine D1 receptor antagonist SCH-23390 blocked these effects of METH, suggesting that NPY levels throughout the nucleus accumbens and the caudate are regulated through D1 pathways. The D2 receptor antagonist eticlopride did not appear to alter the METH effect, but this was difficult to determine because eticlopride decreased NPY levels by itself. A single dose of METH was sufficient to lower NPY levels, in some, but not all, regions examined. The effects on NPY levels after multiple METH administrations were substantially greater and persisted up to 48 h after treatment; this suggests that synthesis of this neuropeptide may be suppressed even after the drug is gone. These findings suggest that NPY systems may contribute to the D1 receptor-mediated effects of the psychostimulants. (+info)
The neuropsychopharmacology of phencyclidine: from NMDA receptor hypofunction to the dopamine hypothesis of schizophrenia. (2/421)Administration of noncompetitive NMDA/glutamate receptor antagonists, such as phencyclidine (PCP) and ketamine, to humans induces a broad range of schizophrenic-like symptomatology, findings that have contributed to a hypoglutamatergic hypothesis of schizophrenia. Moreover, a history of experimental investigations of the effects of these drugs in animals suggests that NMDA receptor antagonists may model some behavioral symptoms of schizophrenia in nonhuman subjects. In this review, the usefulness of PCP administration as a potential animal model of schizophrenia is considered. To support the contention that NMDA receptor antagonist administration represents a viable model of schizophrenia, the behavioral and neurobiological effects of these drugs are discussed, especially with regard to differing profiles following single-dose and long-term exposure. The neurochemical effects of NMDA receptor antagonist administration are argued to support a neurobiological hypothesis of schizophrenia, which includes pathophysiology within several neurotransmitter systems, manifested in behavioral pathology. Future directions for the application of NMDA receptor antagonist models of schizophrenia to preclinical and pathophysiological research are offered. (+info)
Effects of (+)-HA-966, CGS-19755, phencyclidine, and dizocilpine on repeated acquisition of response chains in pigeons: systemic manipulation of central glycine sites. (3/421)The effects of i.m. injections of (+)-HA-966, a glycine-site antagonist at the N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor, its enantiomer (-)-HA-966, the competitive glutamate antagonist CGS-19755, the uncompetitive glutamate antagonists phencyclidine and dizocilpine, and the micro opioid agonist morphine were evaluated in a repeated acquisition task in pigeons. All of the drugs produced dose-dependent decreases in rates of responding. The NMDA receptor and channel blockers and (+)-HA-966 appeared to have a greater effect on acquisition than did morphine at doses that did not fully suppress responding. The rate suppression and learning impairment produced by a large dose of (+)-HA-966 (100 mg/kg) were completely prevented by coadministration of the glycine-site agonist D-serine (560 mg/kg) but not by its enantiomer, L-serine (1000 mg/kg). D-Serine, however, produced incomplete antagonism of the effects of dizocilpine and phencyclidine and failed to alter those of CGS-19755. These findings provide evidence that reducing the activity of the NMDA subtype of the glutamate receptor through pharmacological action at any of three sites produces similar decrements in acquisition, and those produced through antagonism of the glycine site are differentially sensitive to the glycine-site agonist D-serine. (+info)
Clozapine, but not haloperidol, prevents the functional hyperactivity of N-methyl-D-aspartate receptors in rat cortical neurons induced by subchronic administration of phencyclidine. (4/421)Repeated exposure of rats to the psychotomimetic drug phencyclidine (PCP) markedly increased the response of prefrontal cortical neurons to the glutamate agonist N-methyl-D-aspartate (NMDA) relative to agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid. Moreover, acute challenge by PCP produced a significantly reduced block of NMDA-induced current. In addition, the subchronic administration of PCP reduced significantly the paired-pulse facilitation, accompanied by a significant increase of excitatory postsynaptic current variance. These results suggest that repeated exposure to PCP increased evoked release of excitatory amino acids. The enhanced release of excitatory amino acids evoked by NMDA could explain, at least partly, a hypersensitive response to NMDA and a reduced blockade of the NMDA responses by a PCP challenge in rats exposed repeatedly to PCP. Pretreatment with the atypical antipsychotic drug clozapine, but not the typical antipsychotic drug haloperidol, attenuates the repeated PCP-induced effect. Our results support the hypothesis that clozapine may facilitate NMDA receptor-mediated neurotransmission to improve schizophrenic-negative symptoms and cognitive dysfunction. This novel approach is useful for evaluating the cellular mechanisms of action of atypical antipsychotic drugs. (+info)
Rat strain differences in the ability to disrupt sensorimotor gating are limited to the dopaminergic system, specific to prepulse inhibition, and unrelated to changes in startle amplitude or nucleus accumbens dopamine receptor sensitivity. (5/421)Previous studies indicate that a variety of pharmacological agents interfere with the prepulse inhibition of the acoustic startle (PPI) response including phencyclidine (PCP), 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), amphetamine, and apomorphine. Strain differences have been observed in the ability of apomorphine to disrupt PPI, although the degree to which these strain differences occur after administration of nondopaminergic drugs or the degree to which differences can be observed in other models of dopamine (DA) receptor activation has not been elucidated. The present study tested the effects of apomorphine, amphetamine, 8-OH-DPAT, and PCP on PPI in the Sprague Dawley and Wistar rat strains. Because apomorphine disrupts PPI via activation of DA receptors in the nucleus accumbens, apomorphine-induced hyperlocomotion, also a behavioral model of nucleus accumbens DA receptor activation, was measured in both rat strains. Administration of PCP or 8-OH-DPAT attenuated PPI in both strains, whereas apomorphine and amphetamine only attenuated PPI in Wistar rats. The ability of apomorphine to increase motor activity in the absence of a startle-eliciting stimulus was similar in the two strains, as was apomorphine-induced hyperlocomotion. A time course analysis of the effects of apomorphine on startle response in Sprague Dawley rats found that changes in the magnitude of PPI followed changes in basic startle amplitude. Similarly, no apomorphine-induced attenuation of PPI was observed in Sprague Dawley rats after 6-OHDA-induced DA receptor supersensitivity in the nucleus accumbens. These data suggest a dissociation between the effects of DA receptor agonists in PPI and other behavioral models of DA receptor activation. (+info)
Effects of sustained phencyclidine exposure on sensorimotor gating of startle in rats. (6/421)Phencyclidine (PCP), a non-competitive NMDA antagonist with actions at multiple other central nervous system receptors, can cause both acute and lasting psychoses in humans, and has also been used in cross-species models of psychosis. Acute exposure to PCP in rats produces behavioral changes, including a loss of prepulse inhibition (PPI) of the startle reflex, which parallels the loss of PPI observed in schizophrenia patients. Sustained exposure to PCP in rats produces neuropathological changes in several limbic regions and prolonged behavioral abnormalities that may parallel neuropsychological deficits in schizophrenia. It is unclear whether sustained PCP exposure will also produce a loss of prepulse inhibition which parallels the decrease observed in schizophrenia patients. In the present study, we examined changes in PPI during and after sustained PCP administration, using 5-day PCP exposure via subcutaneous osmotic minipumps, or 14-day PCP exposure via repeated intraperitoneal injections. In both forms of drug delivery, PPI was disrupted during, but not after, sustained drug exposure. PPI does not appear to be sensitive to neuropathological effects of sustained PCP exposure. (+info)
Excitatory actions of NMDA receptor antagonists in rat entorhinal cortex and cultured entorhinal cortical neurons. (7/421)We have characterized excitatory effects of non-competitive NMDA receptor antagonists MK-801, PCP, and ketamine in the rat entorhinal cortex and in cultured primary entorhinal cortical neurons using expression of immediate early gene c-fos as an indicator. NMDA receptor antagonists produced a strong and dose-dependent increase in c-fos mRNA and protein expression confined to neurons in the layer III of the caudal entorhinal cortex. Induction of c-fos mRNA is delayed and it is inhibited by antipsychotic drugs. Cultured entorhinal neurons are killed by high doses of MK-801 and PCP but c-fos expression is not induced in these neurons indicating that this in vitro model does not fully replicate the in vivo effects of PCP-like drugs in the entorhinal cortex. Excitatory effects of the NMDA receptor antagonists may be connected with the psychotropic side effects of these drugs and might become a useful model system to investigate neurobiology of psychosis. (+info)
Characterization of interaction of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester with Torpedo californica nicotinic acetylcholine receptor and 5-hydroxytryptamine3 receptor. (8/421)The widely used calcium channel antagonist 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8) has been identified as a noncompetitive antagonist (NCA) and open-channel blocker of both muscle- and neuronal-type nicotinic acetylcholine receptors (AChRs). To further examine the interaction of TMB-8 with the AChR, the compound was tested as a competitor for the binding of two NCAs of the Torpedo californica AChR, phencyclidine and 3-trifluoromethyl-3-(m[125I]iodophenyl)diazirine, for which the binding to the AChR has been pharmacologically well characterized and a channel binding loci has been established. TMB-8 fully inhibited specific photoincorporation of 3-trifluoromethyl-3-(m[125I]iodophenyl)diazirine into the resting AChR channel (IC50 = 3.1 microM) and inhibited high-affinity [3H]phencyclidine binding to the desensitized AChR (IC50 = 2.4 microM). We conclude that TMB-8 is a potent NCA of the nicotinic AChR, interacting with the resting, open-channel, and desensitized channel conformations. TMB-8 was next tested as an inhibitor of the structurally homologous 5-hydroxytryptamine (5-HT)3 receptor (5-HT3R). Using 5-HT3R containing Sf21 cell membranes, TMB-8 completely inhibited specific binding of the radiolabeled 5-HT3R antagonist [3H]GR65630 (Ki = 2.5 microM). Furthermore, TMB-8 antagonized 5-HT-evoked currents of both mouse and human 5-HT3Rs expressed in Xenopus laevis oocytes, and additional analysis was consistent with a competitive antagonistic mechanism of action. These results, taken together, indicate that TMB-8 antagonizes the function of the AChR and 5-HT3R by different mechanisms. Given the sequence similarity and emerging evidence of structural homology in the channels of these two receptors, these results underscore the existence of subtle yet important structural differences in each channel. (+info)
Phencyclidine abuse is the use of the drug in excessive or compulsive quantities, without a valid prescription, or for non-medical reasons. This type of abuse can lead to addiction, long-term cognitive impairment, and other negative consequences.
Signs of phencyclidine abuse may include:
* Increased desire to use the drug despite negative consequences
* Difficulty cutting down or controlling use
* Continued use despite physical or mental health problems
* Spending excessive time using or obtaining the drug
* Neglect of responsibilities and activities due to use
* Increased risk-taking behavior
* Delusions, hallucinations, or a loss of touch with reality
If you suspect that someone you know is abusing phencyclidine, it is important to seek professional help as soon as possible. A medical professional can assess the individual's symptoms and determine the appropriate course of treatment.
Treatment for phencyclidine abuse may include:
* Cognitive-behavioral therapy to address negative thought patterns and behaviors
* Medication to manage withdrawal symptoms or co-occurring disorders
* Support groups to provide a safe and supportive environment for individuals struggling with addiction.
It is important to note that phencyclidine abuse can have serious consequences, including long-term cognitive impairment, memory loss, and an increased risk of psychotic episodes. If you or someone you know is struggling with phencyclidine abuse, it is important to seek professional help as soon as possible. With the right treatment and support, individuals can overcome addiction and achieve a healthier, happier life.
Substance-induced psychoses can be caused by a variety of drugs, including:
* Benzodiazepines (such as diazepam)
* Hallucinogens (such as LSD or psilocybin)
* Inhalants (such as solvents or aerosols)
* Opioids (such as heroin or prescription painkillers)
* Stimulants (such as cocaine or amphetamines)
Substance-induced psychoses can also be caused by certain medical conditions, such as brain injury or infection.
Symptoms of substance-induced psychosis can vary depending on the drug or substance used, but may include:
* Hallucinations (hearing, seeing, or feeling things that are not there)
* Delusions (false beliefs that are not based in reality)
* Disorganized thinking and speech
* Disorganized or catatonic behavior
* Changes in mood, such as depression or anxiety
Substance-induced psychosis can be diagnosed by a mental health professional, based on a combination of the following:
* A thorough medical history and physical examination
* Laboratory tests to rule out other causes of the symptoms
* A mental status examination to assess cognitive function and thought content
* Imaging studies (such as CT or MRI scans) to rule out other causes of the symptoms
Treatment for substance-induced psychosis typically involves stopping the use of the drugs or substances that are causing the symptoms. In some cases, medications such as antipsychotics or antidepressants may be prescribed to help manage symptoms. Behavioral therapy and support groups can also be helpful in addressing the underlying issues that led to the development of the psychosis.
Preventing substance-induced psychosis is often challenging, as it can be difficult to predict which individuals are at risk of developing psychotic symptoms. However, some strategies for prevention include:
* Avoiding the use of drugs or substances that have been linked to psychosis
* Seeking professional help if symptoms of psychosis develop
* Getting support from friends and family
* Participating in therapy and support groups to address underlying issues
It is important to note that substance-induced psychosis can be a serious condition, and seeking medical attention as soon as possible is essential. With appropriate treatment, many individuals are able to recover from the symptoms of psychosis and go on to lead fulfilling lives.
The term "schizophrenia" was first used by the Swiss psychiatrist Eugen Bleuler in 1908 to describe the splitting of mental functions, which he believed was a key feature of the disorder. The word is derived from the Greek words "schizein," meaning "to split," and "phrenos," meaning "mind."
There are several subtypes of schizophrenia, including:
1. Paranoid Schizophrenia: Characterized by delusions of persecution and suspicion, and a tendency to be hostile and defensive.
2. Hallucinatory Schizophrenia: Characterized by hearing voices or seeing things that are not there.
3. Disorganized Schizophrenia: Characterized by disorganized thinking and behavior, and a lack of motivation or interest in activities.
4. Catatonic Schizophrenia: Characterized by immobility, mutism, and other unusual movements or postures.
5. Undifferentiated Schizophrenia: Characterized by a combination of symptoms from the above subtypes.
The exact cause of schizophrenia is still not fully understood, but it is believed to involve a combination of genetic, environmental, and neurochemical factors. It is important to note that schizophrenia is not caused by poor parenting or a person's upbringing.
There are several risk factors for developing schizophrenia, including:
1. Genetics: A person with a family history of schizophrenia is more likely to develop the disorder.
2. Brain chemistry: Imbalances in neurotransmitters such as dopamine and serotonin have been linked to schizophrenia.
3. Prenatal factors: Factors such as maternal malnutrition or exposure to certain viruses during pregnancy may increase the risk of schizophrenia in offspring.
4. Childhood trauma: Traumatic events during childhood, such as abuse or neglect, have been linked to an increased risk of developing schizophrenia.
5. Substance use: Substance use has been linked to an increased risk of developing schizophrenia, particularly cannabis and other psychotic substances.
There is no cure for schizophrenia, but treatment can help manage symptoms and improve quality of life. Treatment options include:
1. Medications: Antipsychotic medications are the primary treatment for schizophrenia. They can help reduce positive symptoms such as hallucinations and delusions, and negative symptoms such as a lack of motivation or interest in activities.
2. Therapy: Cognitive-behavioral therapy (CBT) and other forms of talk therapy can help individuals with schizophrenia manage their symptoms and improve their quality of life.
3. Social support: Support from family, friends, and support groups can be an important part of the treatment plan for individuals with schizophrenia.
4. Self-care: Engaging in activities that bring pleasure and fulfillment, such as hobbies or exercise, can help individuals with schizophrenia improve their overall well-being.
It is important to note that schizophrenia is a complex condition, and treatment should be tailored to the individual's specific needs and circumstances. With appropriate treatment and support, many people with schizophrenia are able to lead fulfilling lives and achieve their goals.
Phencyclidine (data page)
List of dopaminergic drugs
Ketamine in society and culture
Serotonin-norepinephrine-dopamine reuptake inhibitor
1926 in science
Substance use disorder
NMDA receptor antagonist
David Lodge (neuroscientist)
Phencyclidine (PCP)-Related Psychiatric Disorders Differential Diagnoses
Phencyclidine overdose: MedlinePlus Medical Encyclopedia
Phencyclidine (PCP) Forensic ELISA Kit | Diagnostics | Neogen
Phencyclidine - PubMed
Phencyclidine Toxicity - PubMed
Erowid.org: Erowid Reference 5553 : Discriminative stimulus properties of phencyclidine : Poling AD, White FJ, Appel JB
Phencyclidine (PCP) - Clear Results Drug Tests
PCP-S02M (PCP) Phencyclidine Test Device
Effects of pentobarbital and d-amphetamine on oral phencyclidine self-administration in rhesus monkeys<...
PCP) Drug test, Phencyclidine Drug test |FDA-CE| 818-591-3030 USA.
NMAM 5th Edition - Methods by Chemical Name | NIOSH | CDC
Moises Asis cmacc 2009 apitherapy for mental disorders and chemical addictions
How Long Can Drugs Be Detected in Hair Follicle Test? vs. Urine Test
Caffeine Toxicity Clinical Presentation: History, Physical Examination
Toxicology screen: MedlinePlus Medical Encyclopedia
DailyMed - DOXYLAMINE SUCCINATE AND PYRIDOXINE HYDROCHLORIDE tablet, delayed release
Effects of single and repeated phencyclidine administration on the expression of metabotropic glutamate receptor subtype mRNAs...
Effects of the serotonin(2A/2C) receptor agonist and antagonist on phencyclidine-induced dopamine release in rat medial...
ICD-10 Code for Hallucinogen use, unspecified with hallucinogen-induced anxiety disorder- F16.980- Codify by AAPC
MedlinePlus - Search Results for: HOUSE DUST
What Your Hair Says about You in a Drug Test - Concentra
Chapter 921 Section 0022 - 2011 Florida Statutes - The Florida Senate
Addiction | Psychology Today South Africa
A Guantanamo Connection? Documents Show CIA Stockpiled Antimalaria Drugs as 'Incapacitating Agents' - Truthout
Alphabetical Browse | Britannica
NEON Climate Change Internship, Vancouver (PO-00734544) | The Student Conservation Association | Handshake
Erowid.org: MDMA References Database
- [iii] Illicit drugs such as methamphetamine, phencyclidine (PCP) and cocaine accounted for 24% of these deaths. (cdc.gov)
- Clozapine ameliorates epigenetic and behavioral abnormalities induced by phencyclidine through activation of dopamine D1 receptor. (medscape.com)
- Ketamine and Phencyclidine (PCP) Ketamine and phencyclidine are N-methyl-D-aspartate receptor antagonists and dissociative anesthetics that can cause intoxication, sometimes with confusion or a catatonic state. (merckmanuals.com)
- Phencyclidine is similar to KETAMINE in structure and in many of its effects. (bvsalud.org)
- Behavioural effects of neonatal lesions of the medial prefrontal cortex and subchronic pubertal treatment with phencyclidine of adult rats. (bvsalud.org)
- Correlations between phencyclidine-like activity and N-methyl-D-aspartate antagonism: behavioral evidence. (medscape.com)
- Olney JW, Labruyere J, Price MT. Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs. (medscape.com)
- The test is based on the principle of competitive and restrain immunoassay for determination of drug of abuse Phencyclidine (PCP) and its metabolites presence in urine. (gv-medic.com)
- It is designed for qualitative determination of Phencyclidine in human urine specimens above a cut-off level of 25 ng/ml. (elisatestkits.com)
- Positive association of phencyclidine-responsive genes, PDE4A and PLAT, with schizophrenia. (cdc.gov)
- Phencyclidine Rapid Test (Cassette) (Min. (elisatestkits.com)