Brain tissue pathologies in an impactacceleration model of traumatic brain injury in mice
Poster Number
13
Format
Poster Presentation
Faculty Mentor Name
Robert Riger
Faculty Mentor Department
Biological Sciences
Abstract/Artist Statement
Traumatic brain injury (TBI) is a serious problem worldwide, contributing to a considerable number of deaths and permanent disability every year. Often as a result of head injury from sports injuries and car accidents, TBI frequently occurs as closed-head injury without apparent penetrating damage or bleeding, and is accompanied by widely distributed / diffuse neuronal damage and brain edema (fluid leaking out of capillaries). To study the molecular mechanisms of TBI in transgenic animals, we adapted an existing widely used diffuse TBI model for rats, the Marmarou impact-acceleration weight-drop model. Our adapted model is based on the C57/black 6 mouse strain that is widely used to create gene knockout or genetically engineered mice. Live animal experiments were performed in collaboration with researchers at UC Davis Medical Center following animal welfare guidelines and institutionally approved animal use protocols. Drop height and weight combinations were optimized to induce mild, moderate or severe TBI with low incidence of skull fracture. To simulate traumatic injury coinciding with blood loss, hemorrhagic shock was induced by removal of blood in some trials. Mild/Moderate TBI was characterized by convulsions, apnea, 5-15 minutes of unconsciousness, and reversible neurological deficits. In contrast, severe TBI was characterized by irreversible neuronal damage, and a persistent vegetative state requiring mechanical lung ventilation, accompanied by seizures and often followed by death. Diffuse neuronal injury was assessed by observation of cell morphological changes in the hippocampus, cerebral cortex, and white matter areas of brain tissue sections, visualized using histological cresyl violet stain. At 24 hours after TBI, structural differences in neuron cell shape were observed where cell bodies appeared shrunken and axons appeared swollen. Subsequently, at 7 days after injury, brain tissues, especially in the hippocampus, showed evidence of decreased neuronal density due to phagocytic removal of dead neurons by the immune system.
Location
DeRosa University Center, Ballroom
Start Date
25-4-2015 10:00 AM
End Date
25-4-2015 12:00 PM
Brain tissue pathologies in an impactacceleration model of traumatic brain injury in mice
DeRosa University Center, Ballroom
Traumatic brain injury (TBI) is a serious problem worldwide, contributing to a considerable number of deaths and permanent disability every year. Often as a result of head injury from sports injuries and car accidents, TBI frequently occurs as closed-head injury without apparent penetrating damage or bleeding, and is accompanied by widely distributed / diffuse neuronal damage and brain edema (fluid leaking out of capillaries). To study the molecular mechanisms of TBI in transgenic animals, we adapted an existing widely used diffuse TBI model for rats, the Marmarou impact-acceleration weight-drop model. Our adapted model is based on the C57/black 6 mouse strain that is widely used to create gene knockout or genetically engineered mice. Live animal experiments were performed in collaboration with researchers at UC Davis Medical Center following animal welfare guidelines and institutionally approved animal use protocols. Drop height and weight combinations were optimized to induce mild, moderate or severe TBI with low incidence of skull fracture. To simulate traumatic injury coinciding with blood loss, hemorrhagic shock was induced by removal of blood in some trials. Mild/Moderate TBI was characterized by convulsions, apnea, 5-15 minutes of unconsciousness, and reversible neurological deficits. In contrast, severe TBI was characterized by irreversible neuronal damage, and a persistent vegetative state requiring mechanical lung ventilation, accompanied by seizures and often followed by death. Diffuse neuronal injury was assessed by observation of cell morphological changes in the hippocampus, cerebral cortex, and white matter areas of brain tissue sections, visualized using histological cresyl violet stain. At 24 hours after TBI, structural differences in neuron cell shape were observed where cell bodies appeared shrunken and axons appeared swollen. Subsequently, at 7 days after injury, brain tissues, especially in the hippocampus, showed evidence of decreased neuronal density due to phagocytic removal of dead neurons by the immune system.