Rapid upregulation of aromatase mRNA and protein following neural injury in the zebra finch (Taeniopygia guttata).
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.
Peterson
R S
RS
Department of Physiological Science and Laboratory of Neuroendocrinology, Brain Research Institute, University of California Los Angeles, 621 Charles E. Young Drive South, Los Angeles, CA 90095, USA. rsp@ucla.edu
Saldanha
C J
CJ
Schlinger
B A
BA
D000818:Animals; D001141:Aromatase / Q000235:genetics / Q000378:metabolism*; D001253:Astrocytes / Q000201:enzymology / Q000473:pathology; D020197:Head Injuries, Penetrating / Q000201:enzymology* / Q000473:pathology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male; D016548:Prosencephalon / Q000201:enzymology / Q000293:injuries / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism*; D020308:Songbirds; D015854:Up-Regulation
D012333:RNA, Messenger; D001141:Aromatase