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Neuroplasticity — A New Approach to the Pathophysiology of Depression

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Neuroplasticity

Abstract

All available antidepressive-acting molecules are based on the empirical discoveries of the clinical efficacy of two classes of compounds, the tricyclic antidepressants (TCAs) and the monoamine oxidase inhibitors, that have now been used for more than half a century. These compounds have been shown to overcome deficits in serotonin, noradrenaline and possibly dopamine function in the brain. This finding formed the basis for the monoamine hypothesis of depression [1] and subsequent monoamine receptor hypotheses proposing that depressive disorders are caused by a chemical imbalance in the brain, which can be counteracted and corrected by antidepressants. The role of monoamines has long been a central focus of research efforts, and resulted in the development of newer and more specific antidepressant agents, the monoamine reuptake inhibitors, which have the same core mechanisms of action in that they promote central monoaminergic neurotransmission.

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Authors
  1. Eberhard Fuchs
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J. A. Costa e Silva J. P. Macher J. P. Olié

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Fuchs, E. (2011). Neuroplasticity — A New Approach to the Pathophysiology of Depression. In: Costa e Silva, J.A., Macher, J.P., Olié, J.P. (eds) Neuroplasticity. Springer, Tarporley. https://doi.org/10.1007/978-1-908517-18-0_1

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  • DOI: https://doi.org/10.1007/978-1-908517-18-0_1

  • Publisher Name: Springer, Tarporley

  • Print ISBN: 978-1-85873-437-8

  • Online ISBN: 978-1-908517-18-0

  • eBook Packages: MedicineMedicine (R0)

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