The purpose of this study was to develop a bilateral model of frontal cortical contusion in the rat that would demonstrate reproducible deficits typically found after frontal lobe injury in humans. We used a pneumatically controlled cortical impactor to create bilateral contusions of the medial prefrontal cortex (PFC) in adult male Sprague-Dawley rats. Cognitive, neurologic, physiologic, and histopathologic measures were used to evaluate changes caused by the injury. The cognitive task employed the Morris water maze (MWM). Contused rats performed worse than sham-operated controls on measures of time taken to find a submerged platform, distance to the platform, and swim strategy. Neurologic measures revealed impairments of tongue mobility and transient deficits of forelimb placing. Body weights of the contused rats were chronically reduced with respect to controls, indicating that cortical contusion produces disruption in homeostasis. All rats given bilateral PFC contusions developed marked necrotic cavities at the site of impact. The borders surrounding the cavities were heavily lined with astrocytes and ameboid microglia. There was subcortical gliosis in the medial caudate that extended throughout the rostral-caudal length of the caudate-putamen and into the mediodorsal (MD) and ventrolateral (VL) nuclei of the thalamus. The thalamus was also the site of distal transneuronal degeneration. In both the MD and the VL, there was significant neuronal loss in the contused rats as compared with sham-operated controls. This method of bilateral cortical contusion demonstrates clear, reproducible results that would be required for the development of future pharmacologic therapies designed to promote functional recovery.
The present study was designed to determine whether a low dose of acute ethanol administration could attenuate cognitive deficits associated with traumatic brain injury. Adult male rats received oral administration of ethanol or drinking water 2 h prior to surgery to produce a blood ethanol concentration of 100 mg% and then received bilateral contusion injuries of the medial prefrontal cortex. Seven days after surgery, the rats began 10 days of testing for acquisition of spatial localization in the Morris water maze where they were required to find a hidden platform to escape from the water. The results indicate that the rats given ethanol at the time of injury later spent significantly less time searching for the hidden platform than their water-treated counterparts. On a memory probe test given on the final day of testing, in which the platform was removed from the pool, rats given the ethanol spent more time in the area where the platform had been located indicating that they learned its location better than the lesion/water controls. In addition, acute ethanol treatment reduced some of the histopathology that typically occurs following severe contusion of the medial frontal cortex but did not attenuate post-traumatic formation of edema. These results indicate that acute ethanol intoxication can reduce the severity of cognitive impairments caused by contusive traumatic brain injury and support the contention that there is a dose-response relationship of acute ethanol intoxication in the setting of traumatic brain injury.
The present experiment was designed to evaluate and correlate the time course of blood-brain barrier (BBB) integrity and cerebral edema in adult male rats given medial frontal cortex contusions. The effect of sex hormones on BBB integrity in the same injury model was also examined, because previous work has shown that progesterone can reduce cerebral edema (Roof et al., 1993). BBB breakdown was assessed by Evans blue extravasation and albumin immunostaining while edema formation was measured by the wet weight dry weight technique. These processes were examined beginning 2 h and continuing up to 10 days after injury. Our findings show that medial frontal contusion in rats produces changes in cerebral water content and opening of the BBB that endures at least 7 days postinjury. Although pseudopregnancy has been shown to reduce cerebral edema at day 1 postinjury, we did not find any evidence that this hormonal state is associated with BBB repair.
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