Rapid Upregulation of Aromatase mRNA and Protein Following Neural Injury in the Zebra Finch (Taeniopygia guttata)

Abstract

The expression of aromatase (oestrogen synthase) within the vertebrate central nervous system (CNS) is key in the provision of local oestrogens to neural circuits. Aromatase expression appears to be exclusively neuronal under normal conditions. However, some in vitro studies suggest the presence of astrocytic aromatase in songbirds and mammals. Recently, aromatase in reactive astrocytes has been demonstrated in response to neural injury in the mammalian CNS. Since the glial aromatase expression first documented in cultures of the songbird telencephalon may reflect processes similar to those in response to mammalian neural injury, we investigated whether injury alters the pattern of aromatase-expression in the zebra finch, a species with very high levels of forebrain aromatase expression. Adult males received a penetrating neural injury to the right hemisphere and were killed either 24 or 72 h later. Controls were anaesthetized and otherwise unmanipulated. We determined the expression of aromatase mRNA and protein using in situ hybridization and immunocytochemistry, respectively. Both the transcription and translation of aromatase is dramatically upregulated around the lesion site in response to neural injury in the zebra finch forebrain. This effect is robust and rapid, occurring within 24 h of the injury itself. Cells that upregulate aromatase appear to be reactive astrocytes based upon morphology. The hemisphere contralateral to the injury and both hemispheres in control birds showed the normal, exclusively neuronal pattern of aromatase expression. The upregulation of aromatase in astrocytes may provide high levels of oestrogen available to modulate processes such as CNS repair. Injury-induced upregulation of astrocytic aromatase may be a general characteristic of the injured vertebrate brain.

Recent advances in behavioral neuroendocrinology: Insights from studies on birds

“…In mammals and birds, recent studies on the role of cell-specific hormone production in response to neural injury reveal a critical role for steroids in the mitigation of damage. Brain damage results in an upregulation of aromatase in reactive glia, a cell-type that does not express aromatase in the intact homeotherm brain (Garcia-Segura et al, 1999, Peterson et al, 2001. These data suggest that glia switch on the ability to synthesize E 2 in response to neural injury, and indicate a functional role for the glial aromatase expression that was first described in cell cultures of songbird telencephalon .…”

Rapid seasonal-like regression of the adult avian song control system

“…17␤-Estradiol (E 2 ), a metabolite of T, promotes the expression of several antiapoptotic genes (43)(44)(45)(46)(47)(48). In zebra finches, neuronal injury is accompanied by an increase in expression of aromatase, an enzyme that converts T to E 2 (49), and inhibition of aromatase increases apoptosis near the injury (50). These results suggest that T and/or its metabolites may reduce programmed cell death in HVC of songbirds.…”

Hippocampal Synapses Depend on Hippocampal Estrogen Synthesis

“…A key role for aromatase has been described frequently in studies on neuroprotective effects of estrogen (for review, see Azcoitia et al, 2001). For instance, intracerebral administration of fadrozole, another aromatase inhibitor, enhanced kainic acid-induced neurodegeneration in the hippocampus of male rats (Peterson et al, 2001). Aromatase is upregulated in the adult nervous system in different lesion paradigms , as are ERs after brain injury (Dubal et al, 1999).…”