Journal of neurotrauma
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In the clinical setting, skin temperature is both easily evaluated and useful in assessments of sympathetic dysfunction. The present study purposed to observe the serial skin temperature changes of both hindlimbs following several types of sciatic nerve injury (complete transection and ligation model [CTL], crush injury model [CRI], and chronic constriction injury model [CCI]) in Sprague-Dawley rats and, further, to delineate the possible mechanisms through various evaluation methods. The temperature differences between the intact and injured areas (ΔT) on the plantar surface and toes varied among the CTL, CRI, and CCI injury models during the acute stage (7 days post-injury). ⋯ The latency and amplitude of the compound muscle action potential (CMAP) in the involved plantar muscle was not found in the CTL group 4 weeks post-injury, but showed gradual restoration in the CRI and CCI models. Regression analysis revealed that the ΔT in the plantar area and toes were affected only by the CMAP amplitude in the involved plantar muscle; therefore, it can be said that the skin temperature on the injured area after sciatic nerve injury was influenced by the functional status of the involved muscle. Measurement of skin temperature can differentiate mild peripheral nerve injury from moderate-to-severe injuries, although its clinical significance might be limited.
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Journal of neurotrauma · Dec 2012
Carvacrol together with TRPC1 elimination improve functional recovery after traumatic brain injury in mice.
Death of Central Nervous System (CNS) neurons following traumatic brain injury (TBI) is a complex process arising from a combination of factors, many of which are still unknown. It has been found that inhibition of transient receptor potential (TRP) channels constitutes an effective strategy for preventing death of CNS neurons following TBI. TRP channels are classified into seven related subfamilies, most of which are Ca(2+) permeable and involved in many cellular functions, including neuronal cell death. ⋯ To better define the type of the specific channel involved, the effect of carvacrol on the extent and speed of recovery after TBI was compared among mice lacking TRPC1, TRPC3, or TRPC5, relative to wild type controls. We found that neurological recovery after TBI was significantly enhanced by combining carvacrol with TRPC1 elimination, but not by the absence of TRPC3 or TRPC5, showing a synergistic effect between carvacrol application and TRPC1 elimination. We conclude that TRPC1-sensitive mechanisms are involved in TBI pathology, and that inhibition of this channel by carvacrol enhances recovery and should be considered for further studies in animal models and humans.
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Journal of neurotrauma · Dec 2012
Astrocyte-specific expression of survivin after intracerebral hemorrhage in mice: a possible role in reactive gliosis?
Intracerebral hemorrhage (ICH), the most common form of hemorrhagic stroke, accounts for up to 15% of all strokes. Despite maximal surgical intervention and supportive care, ICH is associated with significant morbidity and mortality, in part due to a lack of viable treatment options. Astrogliosis, a key feature of secondary injury that is characterized by glial proliferation, is a poorly-defined process that may produce both beneficial and detrimental outcomes after brain injury. ⋯ Moreover, the survivin expression was co-localized in proliferating astrocytes as evidenced by triple-label immunohistochemistry. Finally, shRNA-mediated silencing of survivin expression attenuated PCNA expression and reduced cellular proliferation in human glial cells. Together, these data suggest a potentially novel role for survivin in functionally promoting astrocytic proliferation after ICH.