Female gonadal hormone effects on microglial activation and functional outcomes in a mouse model of moderate traumatic brain injury.
Repository Usage Stats
AIM: To address the hypothesis that young, gonad-intact female mice have improved long-term recovery associated with decreased neuroinflammation compared to male mice. METHODS: Eight to ten week-old male, female, and ovariectomized (OVX) mice underwent closed cranial impact. Gonad-intact female mice were injured only in estrus state. After injury, between group differences were assessed using complementary immunohistochemical staining for microglial cells at 1 h, mRNA polymerase chain reaction for inflammatory markers at 1 h after injury, Rotarod over days 1-7, and water maze on days 28-31 after injury. RESULTS: Male mice had a greater area of injury (P = 0.0063), F4/80-positive cells (P = 0.032), and up regulation of inflammatory genes compared to female mice. Male and OVX mice had higher mortality after injury when compared to female mice (P = 0.043). No group differences were demonstrated in Rotarod latencies (P = 0.62). OVX mice demonstrated decreased water maze latencies compared to other groups (P = 0.049). CONCLUSION: Differences in mortality, long-term neurological recovery, and markers of neuroinflammation exist between female and male mice after moderate traumatic brain injury (MTBI). Unexpectedly, OVX mice have decreased long term neurological function after MTBI when compared to gonad intact male and female mice. As such, it can be concluded that the presence of female gonadal hormones may influence behavioural outcomes after MTBI, though mechanisms involved are unclear.
Published Version (Please cite this version)10.5492/wjccm.v6.i2.107
Publication InfoUmeano, O; Wang, Haichen; Dawson, Hana Nenicka; Lei, Beilei; Umeano, A; Kernagis, D; & James, Michael Lucas (2017). Female gonadal hormone effects on microglial activation and functional outcomes in a mouse model of moderate traumatic brain injury. World J Crit Care Med, 6(2). pp. 107-115. 10.5492/wjccm.v6.i2.107. Retrieved from http://hdl.handle.net/10161/15423.
This is constructed from limited available data and may be imprecise. To cite this article, please review & use the official citation provided by the journal.
More InfoShow full item record
Adjunct Assistant Professor in the Department of Neurology
Our laboratory studies the role of tau protein in neurodegeneration. Aggregated tau protein is a hallmark feature of a group of neurodegenerative dementias called tauopathies. This group of diseases accounts for a large majority of all dementias and includes Alzheimer's disease, Pick's disease and frontotemporal dementia to name a few. To model tauopathies, we overexpressed normal and mutated human tau protein or no tau protein in the central nervous system of transgenic mice. Several of t
Associate Professor of Anesthesiology
I have an extensive background in neuroanesthesia and neurointensive care and a special research interest in translational and clinical research aspects of intracerebral hemorrhage. After completing residencies in neurology and anesthesiology with fellowships in neurocritical care, neuroanesthesia, and vascular neurology, I developed a murine model of intracerebral hemorrhage in the Multidisciplinary Neuroprotection Laboratories at Duke University. After optimization of the model, I h
Assistant Professor of Neurology
Alphabetical list of authors with Scholars@Duke profiles.