Study of a New Schizophrenomimetic Drug—Sernyl

LUBY, ELLIOT D.

doi:10.1001/archneurpsyc.1959.02340150095011

Cited by 921Schizophrenia research and treatmentNeurotransmitter Receptor Influence on BehaviorHallucinations in medical conditions

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Study of a New Schizophrenomimetic Drug—Sernyl

LUBY, ELLIOT D.·1959·Archives of Neurology And Psychiatry

DOI 10.1001/archneurpsyc.1959.02340150095011

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Abstract

Introduction The production of model psychoses has been employed as a technique for testing hypotheses relevant to the causes, correlates, and treatment of schizophrenia since 1921, when De Jong demonstrated experimental catatonia by giving bulbocapnine to animals.5This method of study has received considerable impetus with the discovery of the hallucinogenic properties of lysergic acid diethylamide (LSD-25)22and other psychotomimetic agents. Objections have since been raised to the drawing of premature analogies between the psychotic-like states produced by drugs and the psychopathology of schizophrenia. Ebaugh has pointed out that "the difference between these pseudopsychoses and schizophrenia is so striking that such experimentation seems to have only tenuous relevance to the problem of schizophrenia."7On the other hand, Wikler has asserted that "from the standpoint of the development of dynamic (causal) concepts about human behavior, it matters little whether or not model psychoses resemble schizophrenia. Drugs which modify

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The hypothesis that NMDAR hypofunction might be a pathogenic trigger for schizophrenia arose from observations that phencyclidine and ketamine mimic primary schizophrenia symptoms in healthy subjects and are NMDAR antagonists.
“The hypothesis that NMDAR hypofunction might be a pathogenic trigger for schizophrenia 9,10 arose from observations that administration of the dissociative anesthetics phencyclidine and ketamine to healthy subjects mimicked the primary symptoms of schizophrenia 11,12 coupled with the finding that these compounds are NMDAR antagonists 13 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [11]

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Authors: LUBY, E. D.
Corresponding author: LUBY, ELLIOT D.
Venue: Archives of Neurology And Psychiatry
Publisher: American Medical Association (AMA)
Published: 1959-03-01
Volume: 81
Issue: 3
Pages: 363
ISSN: 0096-6754 (ISSN-L)
DOI: 10.1001/archneurpsyc.1959.02340150095011
OpenAlex: W2138368199
Cited by: 921
References: 11
Citations by year: 2026: 5 · 2025: 6 · 2024: 8 · 2023: 10 · 2022: 13 · 2021: 10 · 2020: 10 · 2019: 14 · 2018: 21 · 2017: 22 · 2016: 33 · 2015: 31 · 2014: 21 · 2013: 26 · 2012: 34
FWCI: 21.57
Type: journal article
Language: en
Open access: closed
Locations: Archives of Neurology And Psychiatry (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Cognitive Neuroscience › Hallucinations in medical conditions
Keywords: experimental psychosis, schizophrenia, drug-induced psychosis
MeSH terms: Anesthetics, Humans, Phencyclidine, Schizophrenia

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Study of a New Schizophrenomimetic Drug—Sernyl

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