Animal models of schizophrenia
May 15, 2018 DOI: 10.4324/9781315268217-7 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Theoretical or philosophical paper |
|---|---|
| Citations | 1 |
| Key points | Argues that LSD-25 should be reexamined as the basis for an animal model of schizophrenia, contending that schizophrenia is a complex disorder of multiple causation with features likely outside its core defect, and that the perception that amphetamine is a better pharmacological model hastened the decline of interest in LSD. |
Abstract
This chapter argues that the case for reexamining lysergic acid diethylamide (LSD)-25 as the basis for an animal model of schizophrenia. Schizophrenia is a complex natural disorder of multiple causation and has many features which are almost certainly not part of the core defect of the disease. During its relatively brief history LSD-25 has been the subject of controversy even greater than that which usually greets new scientific discovery. In the first category are the various stereotyped behaviors produced by amphetamine psychosis, which some workers have discussed as a chemical model for schizophrenia. The staggering literature on schizophrenia attests to the fact that virtually every single biological or psychological characteristic has been explored. Several investigators have used this principle to explain various perceptual and attentional deficits in schizophrenia. An important factor which undoubtedly hastened the decline of interest in LSD was the view, already mentioned, that amphetamine constituted a better pharmacological model of schizophrenia.