Download or read book Consequences and Mechanism of 3 4 methylenedioxymethamphetamine MDMA induced Serotonin Neurotoxicity written by Mahalakshmi Shankaran and published by . This book was released on 2000 with total page 470 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book MDMA induced serotonergic neurotoxicity written by Dominik Buchmüller and published by GRIN Verlag. This book was released on 2009-10-06 with total page 14 pages. Available in PDF, EPUB and Kindle. Book excerpt: Seminar paper from the year 2009 in the subject Psychology - Biological Psychology, grade: A (100%), New College Durham (Duke University, Department of Psychology and Neuroscience), course: Behavior and Neurochemistry, language: English, abstract: It is the aim of this paper to review and integrate relevant empirical findings and theoretical discussions concerning the molecular and cellular mechanisms and effects of MDMA-induced 5-HT neurotoxicity in laboratory animals. 3,4-methylenedioxymethamphetamine (MDMA) is a derivative of the synthetic psychostimulant methamphetamine (METH). It also shares some structural and pharmacological properties of mescaline, a naturally occurring psychedelic hallucinogen. At the molecular level, all three substances resemble the monoamine neurotransmitters epinephrine (E) and dopamine (DA). They mimic the neurophysiological actions and effects of E and DA, as well as serotonin (5-HT). METH and MDMA do so by binding to, and reversal of monoamine-specific transporter proteins at the presynaptic plasma membrane. While the psychological effects of METH are mainly due its action as a DA release agent and reuptake inhibitor, MDMA primarily affects the serotonergic system. It has a high affinity for the serotonin-specific transporter (SERT), which carries it into the presynaptic neuron. Inside the cell, MDMA inhibits the vesicular monoamine transporter type 2 (VMAT2), pre-venting intracellular 5-HT from being stored in synaptic vesicles. In addition, MDMA phos-phorylates SERT, which causes a reversal of its reuptake function and, hence, non-exocytotic efflux of 5-HT by the means of passive diffusion. Because neurotransmitter release normally only occurs in case of an action potential, and the released transmitter is partly reabsorbed and recycled, the reverse functioning of SERT depletes 5-HT stores. The equivalent effect of METH via reversal of the DA transporter (DAT) has been linked to its neurotoxic properties (Yamamoto & Zhu, 1998). As a derivative of methamphetamine, MDMA is sometimes believed to have inherited the severe dopaminergic neurotoxicity of METH and its parent compound amphetamine. Such neurotoxic potential has been found in mice but not in rats (Colado, O’Shea, and Green, 2004), and remains to be established for non-human primates. The probably most prominent publication claiming that MDMA caused irreversible damage to primate DA neurons (Ricaurte et al., 2002) was shown to be in error and had to be retracted. Instead of a recreational dose of MDMA (3 2 mg/kg), the monkeys had, in fact, been given METH, which, at such doses, is known to be neurotoxic in primates (Villemagne et al., 1998). [...]

Download or read book Studies on the 3 4 Methylenedioxymethamphetamine mdma Induced Dysregulation of Energy Metabolism and Its Neurochemical Consequences written by and published by . This book was released on 2005 with total page 179 pages. Available in PDF, EPUB and Kindle. Book excerpt: 3,4-Methylenedioxymethamphetamine (MDMA), an analog of the amphetamine class, is a psychostimulant and a popular drug of abuse. MDMA is considered to be selectively neurotoxic to serotonergic nerve terminals in different brain regions, however the exact mechanisms through which MDMA produces serotonin (5-HT) neurotoxicity remain unknown. Oxidative stress has been reported to play an important role in mediating this process. In addition to the potential role of oxidative stress in MDMA neurotoxicity, there is evidence that bioenergetic stress may play an important role in the toxicity produced by amphetamine analogs. The overall hypothesis, which provides the basis for the current proposal is that MDMA produces dysregulation of brain energy metabolism and this plays an important role in MDMA-induced neurotoxicity. The effect of MDMA on brain energy metabolism was investigated by examining the effect of MDMA on brain glycogen. MDMA produced a time and dose-dependent decrease in brain glycogen. Maintenance of rats at a cool ambient temperature of 17 0C or pretreatment with 5-HT2 antagonists, significantly attenuated the MDMA-induced hyperthermia and glycogenolysis. However, MDMA-induced hyperthermia, as well as glycogenolysis, was found to be neither sufficient nor necessary for the MDMA-induced long-term 5-HT depletion. Administration of substrates of energy metabolism, e.g., nicotinamide, ubiquinone, attenuated the MDMA-induced long-term 5-HT depletion. Nicotinamide also attenuated the long-term DA and 5-HT depletion produced by coperfusion of MDMA and the mitochondrial inhibitor malonate. A neurotoxic regimen of MDMA produced a significant depletion of ATP in the striatum and hippocampus. Dysregulation of energy metabolism and energy depletion results in increased intracellular Ca2+ levels in the mitochondria, which results in activation of nitric oxide synthase (NOS) and generation of nitric oxide (NO). A neurotoxic regimen of MDMA produced an increase in NO in the striatum. The MDMA and malonate-induced long-term DA and 5-HT depletion were attenuated by administration of NOS inhibitors, as well as a peroxynitrite decomposition catalyst. The neuronal NOS inhibitor S-methyl-L-thiocitrulline (S-MTC) attenuated the MDMA-induced long-term 5-HT depletion without attenuating the MDMA-induced hyperthermia. These results support the conclusion that MDMA produces dysregulation of energy metabolism and this bioenergetic stress contributes to MDMA-induced neurotoxicity.

Download or read book Ecstasy The Clinical Pharmacological and Neurotoxicological Effects of the Drug MDMA written by Stephen J. Peroutka and published by Springer Science & Business Media. This book was released on 2012-12-06 with total page 252 pages. Available in PDF, EPUB and Kindle. Book excerpt: The variety of viewpoints expressed in this book illustrate the many contro versies surrounding MDMA [1]. On the one hand, the proponents ofMDMA use believe this agent offers a unique psychoactive effect that may have important clinical applications, especially in the field of psychotherapy. On the other hand, the scientific data concerning the neurotoxic effects of the drug are unequivocal. The most striking feature of the human information of MDMA is the paucity of data that has been generated on the drug since it was patented in 1914. As pointed out by Beck (Chapter 6) and others, a clear need exists for better epidemiological and clinical data on MDMA. In the absence of such data, arguments both for and against the cotinued use ofMDMA with humans will be difficult to support. Unfortunately, the currently available data must be used to develop rational policies for potential human users of MDMA. At the present time, there are no data indicating that recreational doses of MDMA permanently damage the human brain. Nonetheless, based on a review of the contents of this book as well as on informal discussions with approximately 200 recreational users of MDMA, the following personal observations suggest that MDMA is radically different from other recreational drugs.

Download or read book A Stereotaxic Atlas of the Squirrel Monkey s Brain Saimiri Sciureus written by John A. Gergen and published by . This book was released on 1962 with total page 100 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book The Role of L tyrosine in the Neurotoxicity of 3 4 methylenedioxymethamphetamine MDMA in the Rat and in a Serotonergic Cell Line written by Joseph Michael Breier and published by . This book was released on 2007 with total page 299 pages. Available in PDF, EPUB and Kindle. Book excerpt: Evidence shows that the amphetamine derivative (+)3,4-methylenedioxymethamphetamine (MDMA) is selectively toxic to the serotonin (5-HT) system, but the specific mechanisms underlying MDMA-induced damage to 5-HT neurons remain to be elucidated. A role for dopamine (DA) has been hypothesized but fails to account for 5-HT damage seen in regions sparsely innervated by dopamine nerve terminals. Moreover, there is no evidence that DA directly mediates toxicity to 5-HT terminals in vivo after MDMA. To address how DA contributes to MDMA-induced neurotoxicity, L-tyrosine, the amino acid precursor to DA, was investigated as a potential contributor to 5-HT neuron toxicity. In vivo microdialysis experiments in the rat striatum and hippocampus demonstrate that MDMA increased the extracellular concentration of tyrosine, and that the local addition of tyrosine enhanced the acute increases in extracellular DA and the selective long-term 5-HT depletions after MDMA. These effects were dependent on aromatic amino acid decarboxylase (AADC) but independent of tyrosine hydroxylase (TH). In vitro data showed that tyrosine is non-enzymatically converted to DOPA by hydroxyl radicals. Together, these results led to the hypothesis that cytotoxic DA formed de novo inside 5-HT neurons from MDMA-induced increases in tyrosine can mediate 5-HT terminal damage.

Download or read book Behavioral Toxicology written by Bernard Weiss and published by Springer Science & Business Media. This book was released on 2013-03-09 with total page 475 pages. Available in PDF, EPUB and Kindle. Book excerpt: Behavioral toxicology is a young discipline in the United States; so young, in fact, that this is one of its first books. Behavioral questions are bound to play a major role in future scientific work and governmental decisions involving the health effects of environmental contaminants and other chemicals. This role springs from two key problems that face scientists and public agencies required to set acceptable exposure standards or to determine criteria for the toxicity of therapeutic chemicals: How do you evaluate effects that may show up only as subtle functional disturbances? And how do you de tect toxic effects early enough so that they may still be reversible, before they produce major damage? The contributions in this book come from a collection of scientists whose interests span a wide variety of problem areas. The focus is largely on me thodological issues because they represent the most immediate concern of the discipline. We expect that this collection of papers will represent a useful source book for behavioral toxicology for some time. For the past few years, the University of Rochester's Department of Radiation Biology and Biophysics has sponsored a series of international conferences on chemical toxicity, partly as a response to concern over the con sequences to health of the rich chemical soup in which we live. This book is based upon presentations made to the fifth of the series. Held in June, 1972, it was the first formal meeting devoted to behavioral toxicology in this country.

Download or read book Consequences of 3 4 methylenedioxymethamphetamine MDMA Administration in the Rat written by Megan M. W. Straiko and published by . This book was released on 2006 with total page 182 pages. Available in PDF, EPUB and Kindle. Book excerpt: "3,4-Methylenedioxymethamphetamine (MDMA) is a popular drug of abuse that produces long-term decreases in neurochemical markers of 5-HT that are believed to be indicative of selective toxicity to the 5-HT nerve terminal. A potential mechanism underlying this proposed neurotoxicity involves reactive nitrogen species. In vivo microdialysis studies demonstrated that MDMA increases extracellular nitrite/nitrate (NOx), a marker of NO, and that this is iNOS dependent. However, iNOS-dependent MDMA-induced NOx formation is unrelated to long-term 5-HT toxicity, as iNOS inhibition had no effect on long-term MDMA-induced 5-HT depletion. Histological evidence of MDMA-induced 5-HT nerve terminal damage is inconsistent. Antibodies to the cleaved form of the microtubule associated protein tau (C-tau) were used to characterize neurotoxicity produced by psychostimulant drugs. Amphetamine (AMPH) and methamphetamine (METH), both DA-depleting compounds, produced an increase in C-tau immunoreactivity, whereas the 5-HT-depleting drugs MDMA, para-methoxyamphetamine (PMA) and the prototypic 5-HT neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) did not. C-tau was localized to astrocytes, not neurons, suggesting that C-tau is not a direct marker of neuronal damage, but may be an alternative indicator of reactive gliosis. Furthermore, these data are in agreement with previous findings that AMPH and METH produce reactive gliosis, whereas MDMA, PMA and 5,7-DHT do not. Human users of MDMA have reported cognitive/behavioral deficits following chronic use, including impaired sexual function and reduced sexual motivation. In the rat, prior treatment with MDMA may alter the rewarding properties of other drugs of abuse. Given the potential similarities in neural pathways mediating the rewarding properties of drugs and sex, studies were designed to assess the effect of MDMA on the response to a natural reward, i.e., sex, in the conditioned place preference (CPP) paradigm. Rats treated with a 5-HT-depleting regimen of MDMA exhibited no impairment in sexual function, but failed to form CPP to sex, potentially indicating impairments in the neural circuits mediating sexual reward. These studies indicate that iNOS contributes to MDMA-induced NO formation, but not 5-HT depletion, and that MDMA does not produce an appreciable glial response as indicated by increased C-tau formation. Furthermore, MDMA administration is accompanied by failure to exhibit behavior associated with the rewarding properties of sex.

Download or read book Effects of 3 4 methylenedioxymethamphetamine mdma on Cholinergic Neurons in the Rat Brain written by and published by . This book was released on 2005 with total page 215 pages. Available in PDF, EPUB and Kindle. Book excerpt: 3,4-Methylenedioxymethamphetamine (MDMA), an amphetamine analog, is a psychomotor stimulant and a popular drug of abuse. The effect of MDMA on the release of the monoamine neurotransmitters serotonin (5-HT) and dopamine (DA) has been well documented. In contrast, very little is known about the influence of MDMA on other neurotransmitter systems. In view of feelings of heightened awareness and behavioral arousal in human MDMA users, and the role of the cholinergic system in processing environmental cues following novel and arousing stimuli, the influence of MDMA on acetylcholine (ACh) release was examined in the prefrontal cortex (PFC) and hippocampus. Using in vivo microdialysis, it was determined that MDMA enhances the release of ACh in the PFC and hippocampus, possibly by mechanisms localized to these brain regions. In addition, it was also determined that MDMA-induced release of ACh in the PFC, but not hippocampus, is mediated by serotonergic and dopaminergic mechanisms. Further studies examining the role of various 5-HT and DA receptors in the MDMA-induced release of ACh in the PFC indicate that receptors of the 5-HT4 and D1 subtype mediate the release of cortical ACh induced by MDMA. Whereas MDMA use has been associated with behavioral activation and cortical arousal immediately following drug intake, in the long term the drug is known to produce significant cognitive impairments. In view of the cognitive impairments following MDMA use and administration, and the central role of ACh in attentional processing and cognition, studies were designed to assess the influence of a neurotoxic regimen of MDMA, on the subsequent stimulation of ACh release in the PFC. Prior treatment with a 5-HT depleting regimen of MDMA resulted in decreased ACh release in response to subsequent administration of MDMA. In contrast, treatment with a neurotoxic regimen of MDMA did not significantly alter the subsequent stimulation of ACh release induced by application of tail pinch or by the novelty of an intruder rat. Thus, results from the present study indicate that although a 5-HT depleting regimen appears to inhibit subsequent MDMA-induced ACh release in the PFC, it has little impact on subsequent stimulation of ACh release by physiological stressors.

Download or read book The Effects of Drug Abuse on the Human Nervous System written by Bertha Madras and published by Elsevier. This book was released on 2013-11-15 with total page 625 pages. Available in PDF, EPUB and Kindle. Book excerpt: Drug use and abuse continues to thrive in contemporary society worldwide and the instance and damage caused by addiction increases along with availability. The Effects of Drug Abuse on the Human Nervous System presents objective, state-of-the-art information on the impact of drug abuse on the human nervous system, with each chapter offering a specific focus on nicotine, alcohol, marijuana, cocaine, methamphetamine, MDMA, sedative-hypnotics, and designer drugs. Other chapters provide a context for drug use, with overviews of use and consequences, epidemiology and risk factors, genetics of use and treatment success, and strategies to screen populations and provide appropriate interventions. The book offers meaningful, relevant and timely information for scientists, health-care professionals and treatment providers. - A comprehensive reference on the effects of drug addiction on the human nervous system - Focuses on core drug addiction issues from nicotine, cocaine, methamphetamine, alcohol, and other commonly abused drugs - Includes foundational science chapters on the biology of addiction - Details challenges in diagnosis and treatment options

Download or read book Methods of Behavior Analysis in Neuroscience written by Jerry J. Buccafusco and published by CRC Press. This book was released on 2000-08-29 with total page 341 pages. Available in PDF, EPUB and Kindle. Book excerpt: Using the most well-studied behavioral analyses of animal subjects to promote a better understanding of the effects of disease and the effects of new therapeutic treatments on human cognition, Methods of Behavior Analysis in Neuroscience provides a reference manual for molecular and cellular research scientists in both academia and the pharmaceutic

Download or read book Cognition and Addiction written by Antonio Verdejo García and published by Academic Press. This book was released on 2019-09-29 with total page 442 pages. Available in PDF, EPUB and Kindle. Book excerpt: Cognition and Addiction: A Researcher’s Guide from Mechanisms Towards Interventions provides researchers with a guide to recent cognitive neuroscience advances in addiction theory, phenotyping, treatments and new vistas, including both substance and behavioral addictions. This book focuses on “what to know and “how to apply information, prioritizing novel principles and delineating cutting-edge assessment, phenotyping and treatment tools. Written by world renowned researcher Antonio Verdejo-Garcia, this resource will become a go-to guide for researchers in the field of cognitive neuroscience and addiction. Examines cognitive neuroscience advances in addiction theory, including both substance and behavioral addictions Discusses primary principles of cutting-edge assessment, phenotyping and treatment tools Includes detailed chapters on neuro-epidemiology and genetic imaging

Download or read book The ROLE OF METABOLISM IN ECSTASY MEDIATED SEROTONERGIC NEUROTOXICITY written by Gladys Vanessa Erives Quezada and published by . This book was released on 2009 with total page 342 pages. Available in PDF, EPUB and Kindle. Book excerpt: 3,4-(±)-Methylenedioxymethamphetamine (MDMA) is a synthetic amphetamine derivative commonly used as a recreational drug. Although the selectivity of MDMA for the serotonergic system in rat and humans is well established, the specific mechanism associated with MDMA-induced neurotoxicity is not fully understood. The long-term neurotoxicity of MDMA appears to be dependent upon systemic metabolism since direct administration of MDMA into the brain fails to reproduce the neurotoxic effects seen following peripheral administration, indicating that the parent compound alone is unlikely to be responsible for the neurotoxicity. MDMA is O-demethylenated to the catechol metabolite N-methyl-a-methyldopamine (N-Me-a-MeDA) and demethylated to MDA by cytochrome (s) P450 (CYP450). Thioether (glutathione and N-acetylcysteine) metabolites of N-Me-a-MeDA and a-MeDA are neurotoxic and can be found in rat brain following s.c. injection of MDMA. Because multidose administration of MDMA is typical of drug intake during rave parties, we investigated the effects of multiple doses of MDMA on the concentration of neurotoxic thioether metabolites in rat brain. Administration of MDMA at 12-h intervals for a total of four injections led to a significant accumulation of the N-Me-a-MeDA thioether metabolites in striatal dialysate. In contrast, acute release of 5-HT concentrations was decreased. Since isoenzymes of the CYP2D subfamily (30% metabolism), and the CYP2B or CYP3A1 isoforms, catalyze the low and high KM O-demethylenation reactions, respectively, we subsequently examined the potential role of CYP2D1 in both a genetic and pharmacological model. The data is consistent with the hypothesis that systemic metabolism of MDMA contributes to MDMA-induced serotonergic neurotoxicity via the generation of reactive metabolites. In both the genetic and pharmacological models of CYP2D1 deficiency, attenuation of MDMA-mediated decreases in brain 5-HT concentrations were in the same range (30-40%). Finally, we examined the contribution of various transporters using genetic and pharmacological models to investigate the mechanisms regulating the concentration of thioether metabolites in MDMA neurotoxicity. The data suggest that by regulating various transporters and brain concentrations of the neurotoxic thioether metabolites of MDMA, may subsequently modulate the degree of neurotoxicity. However, further studies are necessary to understand the precise mechanism by which Mrp's and Oat1 transporters modulate MDMA-neurotoxicity. Taken together, these studies are consistent with the view that neurotoxicity of MDMA requires systemic metabolism to form a-MeDA and N-Me-a-MeDA by CYP2D6. Therefore, It is likely that neurotoxicity is mediated by the formation of systemic neurotoxic metabolites.

Download or read book The Role Of Serotonin And Vesicular Monoamine Transporters In The Adverse Responses To Methylenedioxymethamphetamine written by Lucina Eridna Lizarraga-Zazueta and published by . This book was released on 2014 with total page 233 pages. Available in PDF, EPUB and Kindle. Book excerpt: 3,4-(±)-Methylenedioxymethamphetamine (MDMA, Ecstasy) is a widely abused amphetamine derivative with potent stimulant properties. The neuropharmacological effects of MDMA are biphasic in nature. MDMA initially causes synaptic monoamine release, primarily of serotonin (5-HT), producing hyperthermia and hyperactivity (5-HT syndrome). Conversely, the long-term effects of MDMA manifest as a prolonged depletion in 5-HT, and structural damage to serotonergic nerve terminals. Monoamine transporter systems at the plasma membrane and storage vesicles of 5-HT neurons have been implicated in MDMA toxicity. Nonetheless, many mechanistic questions remain regarding the precise role of uptake transporters in MDMA neurotoxicity. The present study was designed to address the importance of the serotonin reuptake transporter (SERT) and the vesicular monoamine transporter 2 (VMAT2) to the physiological, behavioral and neurotoxic responses to MDMA. SERT functions as a primary regulator of 5-HT homeostasis, mediating the reuptake of 5-HT from the synaptic space following its release during neurotransmission. SERT is a molecular target site for MDMA and many antidepressant agents such as the selective serotonin reuptake inhibitor (SSRI) class. Pharmacological inhibition of SERT protects against MDMA-induced serotonergic neurotoxicity. Thus, the effects of MDMA are in part mediated by an ability to interact with and inhibit SERT. Using a SERT-knockout (SERT-KO) rat model, we determined that SERT deficiency modulated the acute toxicities of MDMA, such as hyperthermia and hyperactivity, whilst completely preventing long-term depletions in tissue 5-HT levels, indicating the abolishment of neurotoxicity. Disruption of vesicular monoamine storage via interaction with VMAT2 has also been implicated in MDMA neurotoxicity. VMAT2 participates in the transport of monoamine neurotransmitters, in particular 5-HT and dopamine (DA), into intra-neuronal storage vesicles. As such, VMAT2 is critical in maintaining neuronal health by preventing neurotransmitter oxidation within the cytosol. Pharmacological inhibition of VMAT2 with Ro4-1284 reduced MDMA-induced hyperactivity and averted hyperthermia along with persistent serotonergic deficits. Overall, our results corroborate the hypothesis that SERT and VMAT2 are critical to the in vivo effects of MDMA. Furthermore, given that VMAT2 inhibition diminished the behavioral response to MDMA in rats, pharmacological manipulation of this transporter could be used in the treatment of MDMA abuse and overdose.

Download or read book Neurotoxicology written by Louis W. Chang and published by Elsevier. This book was released on 1995-04-20 with total page 875 pages. Available in PDF, EPUB and Kindle. Book excerpt: Neurotoxicology: Approaches and Methods provides a unique and comprehensive presentation of the current concepts and state-of-the-art methods for the assessment of neurotoxicity. The book analyzes various techniques available and discusses their strengths and weaknesses. This volume will serve as an excellent desk companion and laboratory guide for all investigators, researchers, clinicians, and students interested in neurotoxicology. The internationally knowngroup of editors divide the book into seven sections: Neuromorphological and Neuropathological Approaches; Neurophysiological Approaches; Neurobehavioral Toxicology; Neurochemical and Biomolecular Approaches; In-Vitro Models; Clinical Neurotoxicology; and Risk Assessment of Neurotoxicity. Each section yields the most up-to-date information by experts in their fields. Meticulously organized and edited, Neurotoxicology: Approaches and Methods is the most authoritative and well-planned neurotoxicology book on the market. - Discusses neurobehavioral testing methods for assessment of neural dysfunctions - Explains state-of-the-art diagnostic methods, such as clinico-neuropsychological and neurophysiological methods, for patients confronted by neurotoxic problems - Discusses In Vitro methods, including aggregating brain cell methods, organotypic cultures, and the use of human neuronal cell lines for the assessment of neurotoxicity - Presents step-by-step procedures for many methods - Provides state-of-the-art neuromorphological and biomolecular methods and approaches for neurotoxicity investigation

Download or read book Molecular Basis of Neuropharmacology A Foundation for Clinical Neuroscience written by Eric J. Nestler and published by McGraw Hill Professional. This book was released on 2001-03-28 with total page 570 pages. Available in PDF, EPUB and Kindle. Book excerpt: * The most up-to-date and comprehensive coverage of the relationship of brain function and neuroactive chemicals * Authors are world-known leaders in the field * Molecular Neuropharmacology is the hot topic in medicine

Download or read book The Psychopharmacology of Hallucinogens written by Richard C. Stillman and published by Elsevier. This book was released on 2013-10-22 with total page 349 pages. Available in PDF, EPUB and Kindle. Book excerpt: The Psychopharmacology of Hallucinogens focuses on the properties, compositions, functions, transformations, and reactions of hallucinogens. The selection first offers information on the biosynthesis and action of hallucinogens in mammals; role of biogenic amines in the actions of monomethoxy-amphetamines; and molecular mechanism of action of hallucinogens. The book then takes a look at the molecular determinants for interaction with the LSD receptor, including biological studies, molecular reactivity, and summation of the molecular polarization complexes. The text examines the progress on the development of a receptor model for hallucinogenic amphetamines; characterization of psychotomimetics; physical identification of hallucinogenic compounds; and aspects of the pharmacology of phencyclidine. The book also underscores the effects of LSD, mescaline, and DMT, including effects on humans, proposed model, and effects of monoamine manipulations. The text also presents analysis of hallucinogens by Pavlovian conditioning, behavioral measures of hallucinogenic behavior, and drug model of hallucinosis. The selection is a dependable reference for readers interested in the study of hallucinogens.