Title

Brain tissue pathologies in an impactacceleration model of traumatic brain injury in mice

Poster Number

13

Lead Author Major

Biological Sciences

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

This document is currently not available here.

Share

COinS
 
Apr 25th, 10:00 AM Apr 25th, 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.