Behavioral and EEG Changes Induced by Injection of Schizophrenic Urine Extract

Wada, Juhn A.; Gibson, William C.

doi:10.1001/archneurpsyc.1959.02340180081012

Cited by 20 publications

(6 citation statements)

References 21 publications

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“…The endorphin-like properties of the gluten-derived polypeptides have been well established [77] . These peptides may pass through the blood-brain barrier [78] , influencing behavior, inducing changes in the EEG and determining alterations in neurotransmitter levels [79,80] .…”

Section: Possible Factors Involved In the Association Between CD And mentioning

confidence: 99%

Affective and Psychiatric Disorders in Celiac Disease

Addolorato

Leggio

D’Angelo

et al. 2008

Dig Dis

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Several extraintestinal clinical manifestations have been reported in celiac disease (CD). Among them, growing evidence suggests the association between CD and affective and psychiatric disorders. In this review the most frequent affective and psychiatric disorders associated with CD and the possible mechanisms involved in these associations were analyzed. The available data suggest that screening for CD in patients with affective and/or psychiatric symptoms may be useful since these disorders could be the expression of an organic disease rather than primary psychiatric illnesses.

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Section: Possible Factors Involved In the Association Between CD And mentioning

confidence: 99%

Affective and Psychiatric Disorders in Celiac Disease

Addolorato

Leggio

D’Angelo

et al. 2008

Dig Dis

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“…These were increased; (c) fine undulating membranes could be observed on cell surfaces and the transfer of material from oligodendroglia to neurones became more evident; (d) after some tirhe the granules of liponucleoprotein became smaller and more diffuse and might disappear (LSD also does this). Wada and Gibson (1959) injected extracts from schizophrenic and normal urine into the cerebrospinal fluid of monkeys and cats. The extracts from schizophrenic urine produced a variety of abnormal behaviour patterns-e.g.…”

Section: The Toxicity Of Schizophrenic Body Fluidsmentioning

confidence: 99%

Biochemistry of Schizophrenia

Smythies¹

1963

Postgraduate Medical Journal

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Specific Hypotheses THE last ten years have witnessed an enormous increase in the amount of work carried out in this field and, after many years of disappointment, at long last some positive findings are beginning to emerge. It is too early to make the claim that any definite cause of the illness is known but evidence is now to hand that suggests quite strongly the type of biochemical abnormality that may be involved. Progress in research depends to a great extent on the formulation of adequate hypotheses that can be tested experimentally. The recent progress in schizophrenia research has depended partly on the development of such. hypotheses and partly on ad hoc observations both on the metabolism of schizophrenic patients and on the mode of action of psychotomimetic drugs. The First Specific Hypothesis One key to understanding the biochemical basis of schizophrenia may lie in the chemical formula of the psychotomimetic drugs. These are compounds that can induce in normal people many of the signs and symptoms of an acute schizophrenic illness without causing any delirium or clouding of consciousness. The first such drug to be discovered was mescaline in i886. This is a close relative of adrenaline being 3,4,5-trimethoxyphenylethylamine (Fig. i). This chemical relationship formed the basis of the first specific biochemical theory of schizophrenia published in 1952 by Osmond and Smythies. This theory postulated that schizophrenia might be caused by a derangement of adrenaline metabolism whereby the phenolic hydroxyl groups of the latter would be methylated to form dimethoxyphenylethanolamine (Fig. 2) Recently a fair amount of evidence has accumulated bearing on this hypothesis.(i) It was demonstrated (Axelrod and Tomchick, 1958; Armstrong, McMillan and Shaw, I957) that the normal method of metabolizing adrenaline in the human is by methylating one of the phenolic hydroxyl groups to give metanephrine (Fig. 3) which in turn is deaminated to give VMA.(ii) It was shown by Harley-Mason, Laird and Smythies (I958) that a minor metabolite of mescaline in the human is 3-methoxy-4,5-dihydroxyphenylethylamine (Fig. 3). Thus the metabolites of mescaline and adrenaline are even more alike than their parent substances and one can see how mescaline could act by some interference between its own metabolism and that of adrenaline.(iii) Anxiety-prone individuals, who possess a high level of tone in their sympathetic nervous systems, tend to react more severely to mescaline than do less anxiety-prone individuals and their symptoms are much more akin to those seen in actual schizophrenia. Thus a condition of stimulation of the sympathetic system seems to facilitate the psychotic process. Furthermore the symptomfree relatives of schizophrenic patients react in a much more psychotic (paranoid) manner to LSD than do normal controls.(

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“…Presence of these exorphins in schizophrenic patients is suggested by the finding of increased levels of small peptides in the urine of schizophrenic patients, some of which are neuroactive and display opioid‐like effects (57). These peptides can affect behavior, induce changes in EEG and cause alterations in neurotransmitter levels (58, 59). Specific exorphins which may implicate a link between schizophrenic symptoms and CD include members of the casomorphin family, including β ‐casomorphin‐7.…”

Section: Resultsmentioning

confidence: 99%