Abstract
It has been posited that stressful events may precipitate depression in humans (Abramson et al, 1978; Akiskal and McKinney, 1973; Anisman and Zacharko, 1982a). Alternatively, it is not unlikely that such events may simply exacerbate symptoms in already depressed individuals (Slater and Roth, 1969), or that the response to stressors may be symptomatic of an already existant depression (Hudgens et al. 1967; Morrison et al., 1968). Although it is clear that stressful events may profoundly influence the behavior of animals in various testing paradigms, the mechanisms subserving these behavioral alterations remain to be fully elucidated. Furthermore, there is still some question as to whether these behavioral changes can legitimately be considered as valid models of human depression (Willner, 1985). Among other things, several forms of depression exist, and even in one type of depression the symptoms presented may vary considerably across individuals. Indeed, the view has been expressed that depression may be a biochemically heterogeneous illness, wherein the symptoms may be a consequence of serotonin (5-HT) or norepinephrine (NE) neuronal dysfunction and possibly dopamine (DA) variations as well (Jimerson and Post, 1984; Schildkraut, 1978; van Praag, 1978, 1984).
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Zacharko, R.M., Anisman, H. (1989). Pharmacological, Biochemical, and Behavioral Analyses of Depression: Animal Models. In: Koob, G.F., Ehlers, C.L., Kupfer, D.J. (eds) Animal Models of Depression. Birkhäuser Boston. https://doi.org/10.1007/978-1-4684-6762-8_11
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