Unilateral Cortical Contusion Injury in the Rat: Vascular Disruption and Temporal Development of Cortical Necrosis

Abstract

Cerebrovascular disruption and cortical pathology resulting from either moderate (M-TBI) or severe (S-TBI) traumatic brain injury produced by a pneumatically-driven cortical contusion device were assessed in adult male rats sacrificed at 6 and 24 h or 8 and 30 days after injury to the right sensorimotor cortex. Epidural, subdural, subarachnoid, petechial (cortex and corpus callosum), and/or intraventricular hemorrhage was present in all animals, more extensively and severely following S-TBI. At 6 or 24 h after TBI, acidophilic (acid fuchsin-positive) neurons were numerous and widespread (S-TBI > M-TBI) in the ipsilateral contused cortex. By 8 days few acidophilic neurons were present in peri-impact regions of the ipsilateral neocortex, and none were detected in cortex 30 days postinjury. Both M-TBI and S-TBI groups had enlarged ipsilateral cortical volumes (edema) at 6 and 24 h post-contusion. Eight and 30 days after injury the mean volume of cortical necrosis was significantly larger in S-TBI than in M-TBI rats, and cortical necrosis in both TBI conditions increased between 8 to 30 days postinjury. These results indicate that this pneumatically-driven contusion device produces reliable and consistent primary and secondary cortical histopathology, the extent of which is related to the severity of initial injury.

Voluntary exercise or amphetamine treatment, but not the combination, increases hippocampal brain-derived neurotrophic factor and synapsin I following cortical contusion injury in rats

“…The previously characterized CCI injury device (Sutton et al, 1993;Lindner et al, 1998;Kelly et al, 2000) was used to generate a cortical contusion to the left hemisphere. Each animal was placed under inhalation anesthesia with isoflurane (4% for induction, 2.0% for maintenance, in 100% O 2 at 1.5 l/min).…”

“…The bone flap was removed and the dura left intact in all animals to receive CCI. An electronically controlled pneumatic piston cylinder (Hydraulics Control Inc., Emeryville, CA, USA) mounted onto a stereotaxic micromanipulator (Kopf Instruments, Tujunga, CA, USA) was used to allow for precise localization and control of the impact (Sutton et al, 1993). The piston cylinder was angled 19° away from vertical to allow the flat (5 mm diameter) impactor tip to make contact perpendicular to the brain's surface.…”

Increased cerebral uptake and oxidation of exogenous βHB improves ATP following traumatic brain injury in adult rats

“…The previously characterized CCI injury model (Dixon et al 1991;Sutton et al 1993) was used to generate a focal TBI to the left hemisphere. Following a midline incision, the skull was exposed and a 6-mm diameter craniotomy was drilled over the left hemisphere under a microscope, centered at ) 4 mm anteriorposterior (AP), 5 mm midlateral (ML) relative to bregma.…”

Genetic Manipulation of Cell Death and Neuroplasticity Pathways in Traumatic Brain Injury

“…In contusion brain injuries, rapid local brain deformation causes cell shearing and membrane rupture, resulting in irreversible cell injury and necrosis of affected tissues [7,8]. In penumbral regions where cells undergo delayed neurodegeneration, other mechanisms can dominate, including apoptosis, which is a programmed cell death cascade regulated by effector proteins and caspase protease activation [9,10], and autophagy, which is the lysosomal degradation of components within the cell [11][12][13].…”