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Neurology Research International
Volume 2012 (2012), Article ID 650382, 12 pages
Review Article

Disruption of the Serotonergic System after Neonatal Hypoxia-Ischemia in a Rodent Model

1Royal Brisbane and Women’s Hospital, The University of Queensland, Herston, QLD 4029, Australia
2Clinical Neuroscience, Perinatal Research Centre, The University of Queensland Centre for Clinical Research, Royal Brisbane and Women’s Hospital, The University of Queensland, Herston, QLD 4029, Australia

Received 7 September 2011; Revised 26 October 2011; Accepted 1 November 2011

Academic Editor: Robin L. Haynes

Copyright © 2012 Kathryn M. Buller 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.


Identifying which specific neuronal phenotypes are vulnerable to neonatal hypoxia-ischemia, where in the brain they are damaged, and the mechanisms that produce neuronal losses are critical to determine the anatomical substrates responsible for neurological impairments in hypoxic-ischemic brain-injured neonates. Here we describe our current work investigating how the serotonergic network in the brain is disrupted in a rodent model of preterm hypoxia-ischemia. One week after postnatal day 3 hypoxia-ischemia, losses of serotonergic raphé neurons, reductions in serotonin levels in the brain, and reduced serotonin transporter expression are evident. These changes can be prevented using two anti-inflammatory interventions; the postinsult administration of minocycline or ibuprofen. However, each drug has its own limitations and benefits for use in neonates to stem damage to the serotonergic network after hypoxia-ischemia. By understanding the fundamental mechanisms underpinning hypoxia-ischemia-induced serotonergic damage we will hopefully move closer to developing a successful clinical intervention to treat neonatal brain injury.