Journal of neurotrauma
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Journal of neurotrauma · Sep 2009
Neuropeptide Y modulates c-Fos protein expression in the cuneate nucleus and contributes to mechanical hypersensitivity following rat median nerve injury.
This study sought to investigate the effects of injury-induced neuropeptide Y (NPY) on c-Fos expression in the cuneate neurons and neuropathic pain after median nerve injury. Four weeks after median nerve transection (MNT), the injured nerves stimulated at low intensity (0.1 mA) expressed significantly less NPY-like immunoreactive (NPY-LI) fibers in the cuneate nucleus (CN) than those stimulated at high intensities (1.0 mA and 10 mA). Conversely, a significantly higher number of c-Fos-LI cells were observed in the CN in rats stimulated with 0.1 mA compared to those stimulated with 1.0 mA or 10 mA. ⋯ In rats with median nerve chronic constriction injury (CCI), intracerebroventricular injection of NPY aggravated mechanical allodynia and low-intensity stimulus-evoked c-Fos expression, both of which were reversed by injection of NPY receptor antagonist. However, thermal hyperalgesia was not affected by injection of these two reagents. Taken together, these findings suggest that more NPY release, following low-intensity electrical stimulation of the injured nerve, significantly induces c-Fos expression in the CTNs, which possibly provide the ascending thalamic transmission of neuropathic pain signals.
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Journal of neurotrauma · Aug 2009
Low-level blasts raise intracranial pressure and impair cognitive function in rats.
Brain injury after high-level blast has been established both clinically and experimentally. Less is known about the effects on the brain of exposure to low to moderate blast levels, such as those encountered by military personnel during the firing of weapons. This study investigates if exposure to occupational levels of low-level blasts affect intracranial pressure and cognitive performance. ⋯ After exposure to 10 or 30 kPa and re-testing 2 days later, the latency was increased by over 100%. The results show that exposure of rats to blast levels as low as 10 kPa affects both ICP and cognitive function. Though species differences do not allow direct extrapolation to humans, these findings do pose the question as to whether the thresholds for brain injury might be lower than those of other organs used to set training standards for blast exposure.
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Journal of neurotrauma · Aug 2009
Randomized Controlled TrialProstacyclin treatment in severe traumatic brain injury: a microdialysis and outcome study.
Prostacyclin (PGI(2)) is a potent vasodilator, inhibitor of leukocyte adhesion, and platelet aggregation. In trauma the balance between PGI(2) and thromboxane A(2) (TXA(2)) is shifted towards TXA(2). Externally provided PGI(2) would, from a theoretical and experimental point of view, improve the microcirculation in injured brain tissue. This study is a prospective consecutive double-blinded randomized study on the effect of PGI(2) versus placebo in severe traumatic brain injury (sTBI). All patients with sTBI were eligible. ⋯ verified sTBI, Glasgow Coma Score (GCS) at intubation and sedation of
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Journal of neurotrauma · Aug 2009
Cauda equina repair in the rat: part 1. Stimulus-evoked EMG for identifying spinal nerves innervating intrinsic tail muscles.
Cauda equina injuries may produce severe leg and pelvic floor dysfunction, for which no effective treatments exist. We are developing a rat cauda equina injury model to allow nerve root identification and surgical repair. One possible difficulty in implementing any repair strategy after trauma in humans involves the correct identification of proximal and distal ends of nerve roots separated by the injury. ⋯ Correctly identifying the level of origin of that root was more difficult, but for ventral roots this rate still exceeded 90%. Using the rat cauda equina model, we have shown that stimulus-evoked EMG can be used to identify ventral nerve roots innervating tail muscles with a high degree of accuracy. These findings support the feasibility of using this conceptual approach for identifying and repairing damaged human cauda equina nerve roots based on stimulus-evoked recruitment of muscles in the leg and pelvic floor.
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Journal of neurotrauma · Aug 2009
Conditional knockout of brain-derived neurotrophic factor in the hippocampus increases death of adult-born immature neurons following traumatic brain injury.
It has been reported that the hippocampus is particularly vulnerable to traumatic brain injury (TBI), the consequence of which results in hippocampal-dependent cognitive impairment. In the previous study we found that adult-born immature neurons in the hippocampal dentate gyrus are the most vulnerable cell type to moderate TBI insult. ⋯ The results showed that the amount of adult-born immature neuron death in the hippocampal dentate gyrus significantly increased in the BDNF conditional knockout mice. This result suggests that BDNF is involved in regulating the survival of adult-born immature neurons in the hippocampus following TBI, and potentially might be a useful target for preventing the adult-born immature neurons from death following TBI.