Journal of neurotrauma
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Journal of neurotrauma · Aug 2006
Delayed, post-injury treatment with aniracetam improves cognitive performance after traumatic brain injury in rats.
Chronic cognitive impairment is an enduring aspect of traumatic brain injury (TBI) in both humans and animals. Treating cognitive impairment in the post-traumatic stages of injury often involves the delivery of pharmacologic agents aimed at specific neurotransmitter systems. The current investigation examined the effects of the nootropoic drug aniracetam on cognitive recovery following TBI in rats. ⋯ Drug treatment was terminated during MWM testing on postinjury days 16-20. In this experiment, aniracetam-treated rats did not perform better than vehicle-treated rats. The results of these experiments indicate that aniracetam is an effective treatment for cognitive impairment induced by TBI, even when treatment is delayed for a period of days following injury.
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Journal of neurotrauma · Aug 2006
Differential behavioral and histopathological responses to graded cortical impact injury in mice.
Controlled cortical impact (CCI) injury, a model of contusive brain injury in humans, is being used with increasing frequency in mice to investigate post-traumatic cell damage and death and to evaluate treatment strategies. Because cellular injury mechanisms and therapeutic approaches may depend on the severity of the initial insult, it is important to utilize a model in which outcomes are sensitive to injury severity. Adult male C57Bl/6 mice were anesthetized and subjected to sham injury (n = 23) or CCI injury at either 0.5 mm (n = 22) or 1.0 mm (n = 22) depth of impact at a velocity of 5 m/sec. ⋯ Regional patterns of IgG extravasation and reactive astrocytosis were similar in the two injured groups, but changes were more persistent in the 1.0 mm group. Both levels of injury resulted in acute loss of neuronal MAP-2 immunoreactivity in the cortex and sub-region specific changes in the hippocampus. Thus, increasing the depth of impact led to similar structural alterations in neurons, astrocytes and the vasculature, but resulted in greater behavioral deficits and cortical and hippocampal cell death.
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Journal of neurotrauma · Jul 2006
Comparative StudyActivation of spinal GABA receptors attenuates chronic central neuropathic pain after spinal cord injury.
In this study, we investigated the role of the spinal GABAergic system in central neuropathic painlike outcomes following spinal cord injury (SCI) produced by a spinal hemitransection at T13 of the rat. After SCI, mechanical allodynia develops bilaterally in both hind paws of the rat, lasting longer than 40 days, as evidenced by an increase in paw withdrawal frequency in response to a weak von Frey filament. In naive rats, intrathecal (i.t.) administration in the lumbar spinal cord of GABAA and GABAB receptor antagonists, bicuculline (1-5 microg) and phaclofen (0.1-5 microg), respectively, causes a dose-dependent increase in the magnitude of mechanical allodynia. ⋯ The topical application of muscimol (1 microg) or baclofen (0.5 microg) onto the lumbar cord surface reduce the SCIinduced increased responsiveness of WDR neurons. Inhibitory effects of muscimol and baclofen on both the behavioral mechanical allodynia and the hyperexcitability in WDR neuron with SCI compared to controls, were antagonized by pre-treatment of bicuculline (10 microg) and phaclofen (5 microg), respectively. This study provides behavioral and electrophysiological evidence for the important role of the loss of spinal inhibitory tone, mediated by activation of both GABAA and GABAB receptors, in the development of central neuropathic pain following SCI.
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Journal of neurotrauma · Jul 2006
Comparative StudyCognitive reserve as a resilience factor against depression after moderate/severe head injury.
Depression is one of the most frequently reported and distressing residual complaints in survivors of head injury. Studies investigating the pattern of neuropathology associated with depression post head injury have found little consistency. One explanation for this is that cognitive reserve "protects" against depression either through more efficient processing or more effective compensation. ⋯ A significant difference between depressed and non-depressed survivors was found, with higher intelligence associated with lower rates of depression. No significant anatomical differences were found between depressed and non-depressed survivors. These results suggest that premorbid intelligence may provide a resilience factor against depression in head injury survivors.
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Journal of neurotrauma · Jul 2006
Comparative StudyChanges in cerebral energy metabolites induced by impact-acceleration brain trauma and hypoxic-hypotensive injury in rats.
The aim of this study was to describe, in rats, brain energy metabolites changes after different levels of head trauma (T) complicated by hypoxia-hypotension (HH). Male Sprague Dawley rats (n = 7 per groups) were subjected to T by impact-acceleration with 450-g weight drop from 1.50 or 1.80 m (T 1.50 or T 1.80), or to a 15-min period of HH (controlled hemorrhage to mean arterial pressure [MAP] of 40 mm Hg, and mechanical ventilation with N(2) 90%/O(2) 10%), or to their association (T followed by HH). Invasive MAP, intraparenchymental intracranial pressure (ICP), and cerebral blood flow (CBF using Laser Doppler flowmetry) were recorded during the 5 post-traumatic hours. ⋯ The cerebral perfusion pressure was greater than 70 mm Hg in all groups. The prolonged post-traumatic impairment in brain energy metabolism may be related to traumatic brain injury (TBI) severity. It became worse when T was complicated by HH, but was not related to changes in CBF.