Animal Models in Psychiatry, II - download pdf or read online

By Hymie Anisman, Steve Zalcman, Nola Shanks (auth.), Alan A. Boulton, Glen B. Baker, Mathew T. Martin-Iverson (eds.)

ISBN-10: 0896031772

ISBN-13: 9780896031777

ISBN-10: 159259624X

ISBN-13: 9781592596249

The Animal types in Psychiatry volumes are loosely geared up by means of topic. the 1st quantity features a variety of chapters fascinated with schizophrenia, psyc- ses, neuroleptic-induced tardive dyskinesias, and different d- orders which could contain dopamine, equivalent to realization deficit illness and mania. additionally integrated is a bankruptcy describing a behavioral version for activity-induced anorexia. the second one quantity bargains with affective and nervousness problems, but additionally contains chapters on topics no longer simply labeled as both psychotic, affective, or anxiety-related, comparable to aggression, psychological retardation, and reminiscence issues. 4 chapters on animal versions of schizophrenia or psychoses are integrated in quantity 18 end result of the significance of those issues in psychiatry. Likewise, 3 chapters within the current v- ume care for affective problems, with a fourth bankruptcy on circadian rhythms that still contributes to tools for a- mal types in affective problems. Following the 1st 4 chapters are chapters facing types of hysteria and panic, chapters on aggression, one on psychological retardation, and a last bankruptcy masking reminiscence issues. a few of the behaviorally-based versions of affective issues contain inducing tension in a- mals, often on a protracted foundation. the 1st bankruptcy by means of Anisman, Zalcman, Shanks, and Zacharko describes many of the neurochemical results which are linked to the power program of sensors.

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1983,1986). , 1984) that the sensitivity to DA agonists was augmented in animals that had received repeated immobilization stress, an effect that was prevented by prior administration of naloxone. It was suggested that the acute stressinduced activation of enkephalin activity in the VTA served to release DA neurons from tonic inhibition. , 1988). In addition to the effects of stressors on central opioid release, stressors may affect central opiate receptors. For example, Sirakova et al. , 24 h coupled with food and water deprivation) enhanced 6 opioid receptor binding, with little effect on p receptor binding in rat whole brain.

7. Mean @EM) rate of responding for electrical brain stimulation from the nucleus accumbens in three strains of mice. , 1987). DBA/2J mice, but produced a marked retardation of escape responding in the BALB/cByJ strain. Thus, a particular strain is not generally vulnerable or invulnerable (hardy) to the action of a stressor, but rather the impact of a stressor will be dependent on the specific behavioral task in which animals are tested. Similarly, within a given strain, vulnerability to the effects of a stressor on ICSS is region-specific.

1983). There are several candidates that might act as a mediator between the CNS and immune system. Among others, various pituitary hormones, including ACTH, P-endorphin, prolactin, and growth hormone, are subject to neural modulation and their potential effects may thus be secondary to central neurotransmitter alterations. , 1979). , 1981), and it has been suggested that CN%immune system interactions may be mediated by surface receptors on lymphocytes, which traverse microenvironments richly innervated by autonomic fibers (Williams and Felten, 1981).

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Animal Models in Psychiatry, II by Hymie Anisman, Steve Zalcman, Nola Shanks (auth.), Alan A. Boulton, Glen B. Baker, Mathew T. Martin-Iverson (eds.)


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