Experimental Schizophrenia-Like Symptoms

Rinkel, Max; Deshon, H. Jackson; Hyde, Robert W.; Solomon, Harry C.

doi:10.1176/ajp.108.8.572

Cited by 108 publications

(20 citation statements)

References 2 publications

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“…Subsequent investigations confirmed that administration of mescaline, psilocybin, and LSD induces states that resemble the symptoms of the earliest phases of schizophrenia (Rinkel et al, 1952;Rinkel et al, 1955;Keeler, 1965;Bowers and Freedman, 1966). Indeed, the loss of control over thought processes that occurs after ingestion of psilocybin (Vollenweider et al, 1997b) closely parallels acute psychotic decompensation (Keeler, 1965;Bowers and Freedman, 1966 (McCabe et al, 1972;Freedman and Chapman, 1973).…”

Section: Comparison Of Hallucinogen Effects and Endogenous Psychosesmentioning

confidence: 94%

Serotonin and Schizophrenia

Quednow

Geyer

Halberstadt

2010

Handbook of Behavioral Neuroscience

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Although the serotonin hypothesis of schizophrenia is one of the oldest neurochemical hypotheses on the pathogenesis of this disease, it is still highly topical. The concept of how the serotonin system is involved in the origin and progress of schizophrenia has considerably changed over the past decades. Therefore, the present work will give an overview about the development and the current directions of the serotonin hypothesis of schizophrenia. In this regard, we will discuss the phenomenology of hallucinogenic drug action, model psychosis and translational research, post-mortem studies on receptors and transporters, imaging studies, antipsychotic drug action, neuroendocrine challenge studies, platelet and cerebrospinal fluid data, genetic association studies, developmental aspects, and the cross-talk between the glutamate and the serotonin system. In sum, there are several lines of evidence suggesting that the serotonin system plays a major role in the pathogenesis of at least a subpopulation of schizophrenia patients. Further studies are needed to better characterize patients whose psychotic symptoms are suspected to have a serotonergic origin. Serotonin and Schizophrenia AbstractAlthough the serotonin hypothesis of schizophrenia is one of the oldest neurochemical hypotheses on the pathogenesis of this disease, it is still highly topical. The concept of how the serotonin system is involved in the origin and progress of schizophrenia has considerably changed over the past decades.Therefore, the present work will give an overview about the development and the current directions of the serotonin hypothesis of schizophrenia. In this regard, we will discuss the phenomenology of hallucinogenic drug action, model psychosis and translational research, post-mortem studies on receptors and transporters, imaging studies, antipsychotic drug action, neuroendocrine challenge studies, platelet and cerebrospinal fluid data, genetic association studies, developmental aspects, and the cross-talk between the glutamate and the serotonin system. In sum, there are several lines of evidence suggesting that the serotonin system plays a major role in the pathogenesis of at least a subpopulation of schizophrenia patients. Further studies are needed to better characterize patients whose psychotic symptoms are suspected to have a serotonergic origin.3

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Section: Comparison Of Hallucinogen Effects and Endogenous Psychosesmentioning

confidence: 94%

Serotonin and Schizophrenia

Quednow

Geyer

Halberstadt

2010

Handbook of Behavioral Neuroscience

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“…Many other groups subsequently characterized the effects of LSD, mescaline, and psilocybin and concluded that these hallucinogens produced mental states resembling the earliest phases of schizophrenia (Rinkel et al, 1952, 1955; Osmond and Smythies, 1952; Keeler, 1965; Bowers and Freedman, 1966). Other clinicians, however, noted that differences exist between the effects of hallucinogens and the symptoms of schizophrenia, leading them to question the validity of the model psychosis (Mayer-Gross, 1951).…”

Section: Introductionmentioning

confidence: 99%

Serotonergic hallucinogens as translational models relevant to schizophrenia

Halberstadt

Geyer

2013

International Journal of Neuropsychopharmacology

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One of the oldest models of schizophrenia is based on the effects of serotonergic hallucinogens such as mescaline, psilocybin, and (+)-lysergic acid diethylamide (LSD), which act through the serotonin 5-HT2A receptor. These compounds produce a “model psychosis” in normal individuals that resembles at least some of the positive symptoms of schizophrenia. Based on these similarities, and because evidence has emerged that the serotonergic system plays a role in the pathogenesis of schizophrenia in some patients, animal models relevant to schizophrenia have been developed based on hallucinogen effects. Here we review the behavioral effects of hallucinogens in four of those models, the receptor and neurochemical mechanisms for the effects, and their translational relevance. Despite the difficulty of modeling hallucinogen effects in nonverbal species, animal models of schizophrenia based on hallucinogens have yielded important insights into the linkage between 5-HT and schizophrenia and have helped to identify receptor targets and interactions that could be exploited in the development of new therapeutic agents.

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“…This is the ability of at least one member of each class to cause mental aberrations. Thus, the ergot alkaloid derivative lysergic acid diethylamide produces in man a transient state resembling schizophrenia (Stoll, 1947 ;Fischer et al, 1951 ;Rinkel et al, 1952;Hoch et al, 1952). The harmala alkaloids bearing a methoxyl group cause hallucinations, and so disturb the mental processes of dogs that behaviour becomes noticeably changed.…”

Section: Antimetabolites Of Serotoninmentioning

confidence: 99%