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Animal Models in Psychiatry, I by Paul Willner (auth.), Alan A. Boulton, Glen B. Baker, Mathew

By Paul Willner (auth.), Alan A. Boulton, Glen B. Baker, Mathew T. Martin-Iverson (eds.)

The Animal types in Psychiatry volumes are loosely geared up by means of topic. the 1st quantity features a variety of chapters considering schizophrenia, psyc- ses, neuroleptic-induced tardive dyskinesias, and different d- orders which could contain dopamine, reminiscent of cognizance deficit ailment and mania. the second one quantity bargains with affective and anxiousness problems, but in addition comprises chapters on matters no longer simply labeled as both psychotic, or affective, or an- ety-related, corresponding to aggression, psychological retardation, and reminiscence problems. 4 chapters on animal versions of schizophrenia or psychoses are incorporated within the current v- ume as a result significance of those issues in p- chiatry. Likewise, 3 chapters within the next quantity take care of melancholy. the 1st of the 2 volumes starts off with an introd- tion by way of Paul Willner reviewing the standards for assessing the validity of animal types in psychiatry. He has written - tensively in this topic, and his thorough description of the problems of assorted types of validity offers a framework within which to guage the next chapters. As can be obvious, the remainder chapters in either volumes will refer usually to those concerns. the second one bankruptcy, via Melvin Lyon, describes lots of diversified approaches which were p- posed as strength animal types of schizophrenia. it is a departure from the standard structure, such as distinct - scriptions of particular models.

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An important characteristic of any model must be that the symptoms produced are ameliorated by neuroleptic drugs, which, in the main, are antidopaminergic in function. , 1990). As a result of these disagreements, and also because of the significant modulating effects on DA systems caused by other neurotransmitters and neuromodulators, it is necessary to consider multiple causative factors in the neurochemistry of schizophrenia. Eds. From: A. Boulton, Neuromethods, G. Baker, Vol. 78: Animal Models in Psychiatry I and M.

He has suggested that instead of the “dopamine hypothesis” of schizophrenia, one should speak of the “dopamin+GABA hypothesis,” since many, if not all, of the critical behaviors associated with the DA hypothesis are dependent in part on a GABA-DA interaction. Two particular aspects of this research are of interest here. The first is related to the topographic organization of GABA systems within the corpus striatum and the nucleus accumbens, and the second relates to the effects of GABA within the ventral tegmental area of the mesencephalon.

Miller W. , Rose&i R. , and Seligman M. E. P. (1977) Learned helplessness and depression, in Psychopathology: Animal Models (Maser J. D. and Seligman M. E. ), Freeman, San Francisco, pp. 104-130. 22 Wiher Montgomery A. M. J. ), Cambridge University Press, Cambridge, pp. 177-214. , Sampson D, and WiUner I?. (1990) Dopaminergic mechanism of imipramine action in an animal model of depression. Biol. Psychiat. , and Liebman J, (1981) Delayed emergence of antidepressant efficacy following withdrawal in olfactory bulbectomized rats.

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