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Abstract
Alterations in catecholamine levels and neurotransmission have been shown in depressive
disorders. However, the exact sites of alterations and the relation between these
alterations to the etiology of the disease and the effectiveness of antidepressant
therapy are poorly understood. In this study, catecholamine levels and metabolism
were measured in specific brain regions of a genetic rat model of depression [Flinders
Sensitive Line (FSL) rats], and compared to normal Sprague-Dawley rats. Norepinephrine
levels were found to be two to threefold higher in the nucleus accumbens, prefrontal
cortex, hippocampus and median raphe nucleus of FSL rats as compared with control
Sprague-Dawley rats. Dopamine levels were sixfold higher in the nucleus accumbens
and twofold higher in the striatum, hippocampus and hypothalamus of FSL rats as compared
with control Sprague-Dawley rats. After chronic treatment with the antidepressant
desipramine, the immobility score in a swim test, as a measure of a behavioral deficit,
as well as catecholamine levels of the FSL rats became normalized, but these parameters
in the control rats did not change. The results indicate that the behavioral deficits
expressed in the FSL model for depression correlate with increased catecholamine levels
in specific brain sites, and further suggest the FSL rats as a model for elucidation
of the molecular mechanism of clinically used antidepressant drugs.