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CRF-GLUTAMATE INTERACTIONS IN DEPRESSION: PATHOPHYSIOLOGY AND BEHAVIOURAL DISTURBANCES

By E.H.S. Schut

Abstract

Major depressive disorder (MDD) is a psychiatric disorder characterised by depressed mood, loss of interest or pleasure in daily activities (anhedonia), psychomotor retardation and abnormalities in sleep and appetite. The traditional monoamine hypothesis of depression states that depression results from reduced transmission of particularly serotonin (5HT) and norepinephrine (NE). However, enhanced levels of corticotrophin releasing hormone (CRF) and hypercortisolism have been found in patients with depression, suggesting a role of CRF and the hypothalamic-pituitary-adrenal (HPA) axis in depression. In addition, glutamate has become more interesting in the study of depression, namely because of the finding that N-Methyl-D-aspartate (NMDA) receptor antagonist ketamine provides immediate relieve of depression and depression-like symptoms in both clinical and preclinical studies. Several lines of research suggest that CRF-glutamate interactions establish stress-and anxiety-related responses and may therefore play an important role in depression. The relationship between glucocorticoids and glutamate transmission in depression has led to the hypothesis of neuroplasticity, which argues that abnormal accumulations of glutamate induced by stress result in morphological and structural changes in distinct brain areas that are associated with depression. However, recent studies do not focus on the specific role of CRF in neuroplasticity and how its interaction with glutamate exerts effects that may lead to altered neuroplasticity and depression-like symptoms. Therefore, in this thesis we will discuss how CRF-glutamate interactions might underlie pathophysiology and behavioural disturbances in depression

Topics: depression, stress, CRF, glutamate, neuroplasticity
Year: 2012
OAI identifier: oai:dspace.library.uu.nl:1874/256083
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