Abstract
<h3>Introduction</h3> 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.<sup>5</sup>This method of study has received considerable impetus with the discovery of the hallucinogenic properties of lysergic acid diethylamide (LSD-25)<sup>22</sup>and 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."<sup>7</sup>On 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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