disruption of the serotonergic system after neonatal hypoxia-ischemia in a rodent model

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2012
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Abstract
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.
Reference Key
buller2012neurologydisruption Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Kathryn M. Buller;Julie A. Wixey;Hanna E. Reinebrant
Journal Clinical oral investigations
Year 2012
DOI
10.1155/2012/650382
URL
http://dx.doi.org/10.1155/2012/650382
Keywords
neurology diseases of the nervous system

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