title: Aromatase expression and cell proliferation following injury of the adult zebra finch hippocampus.
abstract: Estrogens can be neuroprotective following traumatic brain injury. Immediately after trauma to the zebra finch hippocampus, the estrogen-synthetic enzyme aromatase is rapidly upregulated in astrocytes and radial glia around the lesion site. Brain injury also induces high levels of cell proliferation. Estrogens promote neuronal differentiation, migration, and survival naturally in the avian brain. We suspect that glia are a source of estrogens promoting cell proliferation after neural injury. To explore this hypothesis, we examined the spatial and temporal relationship between glial aromatase expression and cell proliferation after neural injury in adult female zebra finches. Birds were ovariectomized and given a blank implant or one filled with estradiol; some birds were also administered an aromatase inhibitor or vehicle. All birds received penetrating injuries to the right hippocampus. Twenty-four hours after lesioning, birds were injected once with BrdU to label mitotically active cells and euthanized 2 h, 24 h, or 7 days later. The brains were processed for double-label BrdU and aromatase immunocytochemistry. Injury-induced glial aromatase expression was unaffected by survival time and aromatase inhibition. BrdU labeling was significantly reduced at 24 h by ovariectomy and by aromatase inhibition; effects were partially reversed by E2 replacement. Irrespective of ovariectomy, the densities of aromatase immunoreactive astrocytes and BrdU-labeled cells at known distances from the lesion site were highly correlated. These data suggest that injury-induced glial aromatization may influence the reorganization of injured tissue by providing a rich estrogenic environment available to influence cellular incorporation.
authors.affiliation: Department of Physiological Science, University of California, Los Angeles, CA 90095, USA.
authors.forename: R Scott
authors.initials: RS
authors.lastname: Peterson
authors.forename: Gowry
authors.initials: G
authors.lastname: Fernando
authors.forename: Lainy
authors.initials: L
authors.lastname: Day
authors.forename: Timothy A
authors.initials: TA
authors.lastname: Allen
authors.forename: Jeanette D
authors.initials: JD
authors.lastname: Chapleau
authors.forename: Jenny
authors.initials: J
authors.lastname: Menjivar
authors.forename: Barney A
authors.initials: BA
authors.lastname: Schlinger
authors.forename: Diane W
authors.initials: DW
authors.lastname: Lee
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001141:Aromatase / Q000378:metabolism*; D047072:Aromatase Inhibitors / Q000494:pharmacology; D001930:Brain Injuries / Q000473:pathology* / Q000503:physiopathology; D001973:Bromodeoxyuridine / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D002531:Cerebellum / Q000473:pathology; D004347:Drug Interactions; D004958:Estradiol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology; D017316:Fadrozole / Q000494:pharmacology; D005260:Female; D046369:Finches; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects / Q000502:physiology*; D006624:Hippocampus / Q000201:enzymology / Q000473:pathology*; D010052:Ovariectomy / Q000379:methods; D013997:Time Factors