Title

Neural pathologies in an impactacceleration model of traumatic brain injury in mice

Poster Number

23

Lead Author Major

Biological Sciences

Format

Poster Presentation

Faculty Mentor Name

Robert Rigor

Faculty Mentor Department

Biological Sciences

Abstract/Artist Statement

Traumatic brain injury (TBI) is a devastating problem worldwide that contributes to permanent disability and an estimate of 52,000 deaths annually in the United States. TBI frequently occurs as a closed-head injury due to sports and car accidents, and typically without any penetrating damage or bleeding. The pathophysiology of this injury demonstrates diffuse neuronal damage and brain edema. To study the molecular mechanisms responsible for neuronal damage associated with TBI, we adapted the Marmarou impact-acceleration weight-drop model in C57/black6 transgenic mice. Drop height and weight combinations were optimized to induce mild, moderate or severe TBI with low incidence of skull fracture. 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 accompanied by seizures, often followed by death. Diffuse neuronal injury was assessed by the presence of positive degenerating neurons in the hippocampus, cerebral cortex, and white matter areas of the brain, labeled with histological Fluro-Jade stain. This degeneration was further supported by the observation of cell morphological changes visualized using cresyl violet stain. We have successfully designed and physiologically analyzed a reproducible impactacceleration model of traumatic brain injury in transgenic mice.

Location

DeRosa University Center, Ballroom

Start Date

30-4-2016 10:00 AM

End Date

30-4-2016 12:00 PM

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Apr 30th, 10:00 AM Apr 30th, 12:00 PM

Neural pathologies in an impactacceleration model of traumatic brain injury in mice

DeRosa University Center, Ballroom

Traumatic brain injury (TBI) is a devastating problem worldwide that contributes to permanent disability and an estimate of 52,000 deaths annually in the United States. TBI frequently occurs as a closed-head injury due to sports and car accidents, and typically without any penetrating damage or bleeding. The pathophysiology of this injury demonstrates diffuse neuronal damage and brain edema. To study the molecular mechanisms responsible for neuronal damage associated with TBI, we adapted the Marmarou impact-acceleration weight-drop model in C57/black6 transgenic mice. Drop height and weight combinations were optimized to induce mild, moderate or severe TBI with low incidence of skull fracture. 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 accompanied by seizures, often followed by death. Diffuse neuronal injury was assessed by the presence of positive degenerating neurons in the hippocampus, cerebral cortex, and white matter areas of the brain, labeled with histological Fluro-Jade stain. This degeneration was further supported by the observation of cell morphological changes visualized using cresyl violet stain. We have successfully designed and physiologically analyzed a reproducible impactacceleration model of traumatic brain injury in transgenic mice.