Traumatized and inflamed — But resilient: Glial aromatization and the avian brain
Publication Type: |
Journal Article |
Year of Publication: |
2013 |
Authors: |
Kelli A. Duncan, Bradley J. Walters, Colin J. Saldanha |
Publication/Journal: |
Hormones and Behavior |
Keywords: |
aromatase, avian, injury, neuroprotection |
ISBN: |
0018-506X |
Abstract:
This article is part of a Special Issue “Hormones & Neurotrauma”. Steroids like estrogens have potent effects on the vertebrate brain, and are provided to neural targets from peripheral and central sources. Estradiol synthesized within the vertebrate CNS modulates neural structure and function, including the pathways involved in neuroprotection, and perhaps, neural repair. Specifically, aromatase; the enzyme responsible for the conversion of testosterone to estradiol, is upregulated in the avian and mammalian brain following disruption of the neuropil by multiple forms of perturbation including mechanical injury, ischemia and excitotoxicity. This injury induced aromatase expression is somewhat unique in that it occurs in astroglia rather than neurons, and is stimulated in response to factors associated with brain damage. In this review, we focus on the induction, expression and consequences of glial aromatization in the songbird brain. We begin with a review of the anatomical consequences of glial estrogen provision followed by a discussion of the cellular mechanisms whereby glial aromatization may affect injury-induced neuroplasticity. We then present the current status of our understanding regarding the inductive role of inflammatory processes in the transcription and translation of astrocytic aromatase. We consider the functional aspects of glial aromatization before concluding with unanswered questions and suggestions for future studies. Birds have long informed us about fundamental questions in endocrinology, immunology, and neuroplasticity; and their unique anatomical and physiological characteristics continue to provide an excellent system in which to learn about brain trauma, inflammation, and neuroprotection.