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Neural Plasticity
Volume 2014, Article ID 723915, 14 pages
http://dx.doi.org/10.1155/2014/723915
Review Article

Hippocampal Neurogenesis and Antidepressive Therapy: Shocking Relations

1Paracelsus Medical University, Institute of Experimental Neuroregeneration, Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Strubergasse 22, 5020 Salzburg, Austria
2Paracelsus Medical University, Institute of Molecular Regenerative Medicine, Spinal Cord Injury and Tissue Regeneration Center Salzburg (SCI-TReCS), Strubergasse 22, 5020 Salzburg, Austria
3University Clinics of Psychiatry and Psychotherapy I, Paracelsus Medical University, Ignaz-Harrer-Straße 79, 5020 Salzburg, Austria

Received 31 January 2014; Accepted 25 April 2014; Published 22 May 2014

Academic Editor: Paul Lucassen

Copyright © 2014 Peter Rotheneichner et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Speculations on the involvement of hippocampal neurogenesis, a form of neuronal plasticity, in the aetiology of depression and the mode of action of antidepressive therapies, started to arise more than a decade ago. But still, conclusive evidence that adult neurogenesis contributes to antidepressive effects of pharmacological and physical therapies has not been generated yet. This review revisits recent findings on the close relation between the mode(s) of action of electroconvulsive therapy (ECT), a powerful intervention used as second-line treatment of major depression disorders, and the neurogenic response to ECT. Following application of electroconvulsive shocks, intricate interactions between neurogenesis, angiogenesis, and microglia activation, the hypothalamic-pituitary-adrenal axis and the secretion of neurotrophic factors have been documented. Furthermore, considering the fact that neurogenesis strongly diminishes along aging, we investigated the response to electroconvulsive shocks in young as well as in aged cohorts of mice.