Department of Psychiatry, University of Iowa Carver College of Medicine, Iowa City, Iowa
Department of Neurology, University of Iowa Carver College of Medicine, Iowa City, Iowa
Department of Free Radical and Radiation Biology Program, Department of Radiation Oncology Comprehensive Cancer Center, University of Iowa Carver College of Medicine, Iowa City, Iowa
Department of Veterans Affairs, University of Iowa Carver College of Medicine, Iowa City, Iowa
Pappajohn Biomedical Institute, Iowa Neuroscience Institute, University of Iowa Carver College of Medicine, Iowa City, Iowa

Abstract

Diffuse activation of interleukin-1 inflammatory cytokine signaling after traumatic brain injury (TBI) elicits progressive neurodegeneration and neuropsychiatric dysfunction, and thus represents a potential opportunity for therapeutic intervention. Although interleukin (IL)-1α and IL-1β both activate the common type 1 IL-1 receptor (IL-1RI), they manifest distinct injury-specific roles in some models of neurodegeneration. Despitean induction chamber before being transferred to a nose cone where IV cap was removed and any air bubbles in the hub were also removed. Once deeply anesthetized, mice were connected to the FPI device via 20-inch IV tubing and placed on their right side. A pendulum was released from an angle of 11–12 degrees against the fluid reservoir, generating a brief fluid pulse against the exposed dura. A Tektronix digital oscilloscope (TDS460A) was then used to measure the duration and peak pressure of the fluid pulse. After injury, mice were placed on their backs, and their righting time was measured as an indicator of injury severity. After righting, mice were re-anesthetized with 1%–2% isoflurane, the Luer-Lock hub was removed, and the skin incision was sutured closed. Mice