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Effects of early rearing environment on cortical and limbic activity in the rat: validation of an animal model of depression

Objectif

Depression is a devastating mental illness associated with extremely high social and economic costs, given that the lifetime prevalence of this debilitating disease can be as high as 15%. Characterized byseveral emotional and cognitive disturbances, this d isease can also be fatal as a significant proportion ofits sufferers commit suicide. Although treatments are available for depression, many of its sufferers do not respond adequately to currently available antidepressant drugs. Furthermore, these drugs oft en have unwanted side effects and the onset of their therapeutic effects can take several weeks, highlighting the need for development of more effective antidepressant drug treatments. When studying mental illness, researchers use animal models to replicat e certain features of a disorder to study its possible biological causes, allowing them to develop specific treatments for the disease. In humans, early life trauma is associated with an increased risk of developing depression in adulthood. Similarly, stud ies in rats indicate that stress in early life leads to later changes in biology and behaviour that resemble symptoms of depression; moreover, some of these changes can be reversed by antidepressant drugs. Recent studies have shown that depressed patients have abnormal activity in brain regions involved in emotion and cognition, that activity in these areas is linked in a complex manner, and that these abnormalities can be ameliorated by successful antidepressant drug treatment. Thus, the current project pr oposes to study, in rats, a) the effects of early life stress on activity in these brain regions, b) the relationship between activity in these different areas, and c) the effects of antidepressant drugs on brain activity after early life stress. These stu dies will enhance our understanding of brain function in depression, which may lead to the discovery of better treatments for this disease.

Appel à propositions

FP6-2002-MOBILITY-7
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Coordinateur

THE UNIVERSITY OF NOTTINGHAM
Contribution de l’UE
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