Abstract
The neurochemical model of depression, based on monoaminergic theories, does not allow on its own to understand the mechanism of action of antidepressants. This approach does not explain the gap between the immediate biochemical modulations induced by antidepressants and the time required for their clinical action. Several hypotheses have been developed to try to explain more precisely the action of these molecules, each of them involving mechanisms of receptor regulation. At the same time, data on the neuroanatomy of depression converge toward the existence of specific lesions of this pathology. This chapter aims to provide an overview of recent advances in understanding the mechanisms of neural plasticity involved in pathophysiology depression and in its treatment.
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