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Effects of Androgen Availability on the Activation of Neuroprotective Pathways Following Traumatic Brain Injury

Following traumatic brain injury (TBI), steroid hormones are neuroprotective. Specifically, estrogens decrease apoptotic signaling, neuroinflammation, oxidative stress, and have been shown to normalize glutamate concentrations. Furthermore, androgens also regulate neuroinflammation and mediate gliosis. However, the mechanisms underlying these influences are poorly understood. Cyclooxygenase (COX‐2) and prostaglandin E2 (PGE2) activation appear to be necessary for the injury induced upregulation of estrogen synthesis. This sex specific increase in estrogens promotes neuroprotection by increasing estrogen receptor‐α dependent decreases in neuroinflammation presumably by altering the activity of protein kinase A (PKA) or phosphoinositide‐3‐kinase (PI3K). While there is a considerable amount known about the role of estrogens in this pathway, very little is known about how androgens interact with estrogens to promote neuroprotection. The goal of this study was to further investigate the effect of androgens specifically, but also to identify if there are any interactions between androgens and estrogens on the activation of the COX‐2/PGE2 pathway. Prior to the concussive injury protocol, adult male and female zebra finches (Taeniopygia guttata) were implanted with androgens or an androgen antagonist (flutamide) and collected 1 week later. Activation of the COX‐2/PGE2 pathway was measured using analysis of quantitative polymerase chain reaction and immunohistochemistry. Preliminary data suggest that androgens are involved in estrogen mediated neuroprotection following injury and suggest a novel role for androgens following TBI.