Neuroscience letters
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Neuroscience letters · Sep 2014
Test-retest reliability of thermal quantitative sensory testing on two sites within the L5 dermatome of the lumbar spine and lower extremity.
Quantitative sensory testing (QST) is widely used in human research to investigate the integrity of the sensory function in patients with pain of neuropathic origin, or other causes such as low back pain. Reliability of QST has been evaluated on both sides of the face, hands and feet as well as on the trunk (Th3-L3). In order to apply these tests on other body-parts such as the lower lumbar spine, it is important first to establish reliability on healthy individuals. The aim of this study was to investigate intra-rater reliability of thermal QST in healthy adults, on two sites within the L5 dermatome of the lumbar spine and lower extremity. ⋯ In healthy adults, thermal QST on the lumbar spine and lower extremity demonstrated fair-to-excellent test-retest reliability.
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Neuroscience letters · Sep 2014
Enhanced scratching elicited by a pruritogen and an algogen in a mouse model of contact hypersensitivity.
Chemical pruritogens and algogens evoke primarily itch and pain, respectively, when administered to the skin of healthy human subjects. However, the dominant sensory quality elicited by an algesic chemical stimulus may change in patients with chronic itch where bradykinin, elicits itch in addition to pain. Here we tested whether normally pruritic and algesic chemicals evoked abnormal itch- or pain-like behaviors in the mouse after the development of contact hypersensitivity (CHS), an animal model of allergic contact dermatitis. ⋯ In comparison with responses of control mice, CHS mice exhibited a significant increase in the scratching evoked by bovine adrenal medulla 8-22, a peptide that elicits a histamine-independent itch, but did not alter the scratching to histamine. Bradykinin, an algogen that elicited only wiping in control mice, additionally evoked significant scratching in CHS mice. Thus, within an area of CHS, histamine-independent itch is enhanced and chemically evoked pain is accompanied by itch.
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Neuroscience letters · Sep 2014
Intracerebral interleukin-10 injection modulates post-ischemic neuroinflammation: an experimental microarray study.
Stroke induces a profound neuroinflammatory reaction that leads to secondary cerebral tissue injury. Interleukin-10 (IL-10) is a key anti-inflammatory cytokine that is endogenously produced by immune cells and limits this inflammatory reaction. Previously, therapeutic administration of IL-10 has been shown to be neuroprotective in experimental stroke. ⋯ The microarray analysis revealed that IL-10 treatment effectively downregulated pro-inflammatory signaling cascades which were upregulated by the ischemic lesion in the acute phase after the stroke. This is the first study characterizing the global gene regulation profile of IL-10 immunotherapy for ischemic stroke. Our results emphasize the key role of IL-10 as a neuroprotective cytokine and suggest several novel downstream pathways for further investigation to better understand the mechanisms of post-stroke neuroinflammation.
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Neuroscience letters · Sep 2014
Ursolic acid reduces oxidative stress to alleviate early brain injury following experimental subarachnoid hemorrhage.
Ursolic acid (UA), a well-known anti-oxidative reagent, has been reported to protect the brain against ischemic stoke. However, the potential role of UA in protecting against early brain injury (EBI) after subarachnoid hemorrhage (SAH) remains unclear. The present study aimed to examine the effect of UA against EBI following SAH, and to demonstrate whether the effect is associated with its powerful antioxidant property. ⋯ The endovascular puncture model was used to induce SAH and all the rats were subsequently sacrificed at 48h after SAH. The results show that UA administration could significantly attenuate EBI (including brain edema, blood-brain barrier disruption, neural cell apoptosis, and neurological deficient) after SAH in rats and up-regulate the antioxidative levels in the rat cerebral cortex, suggesting that administration of UA in experimental SAH rats could alleviate brain injury symptom, potentially through its powerful antioxidant property. Hence, we concluded that UA might be a novel therapeutic agent for EBI following SAH.
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Neuroscience letters · Sep 2014
The expression of calcium/calmodulin-dependent protein kinase II in the dorsal horns of rats with type 1 and type 2 diabetes.
The activation of calcium/calmodulin-dependent protein kinase II (CaMKII) has been proposed as a key factor in chronic pain development. This study therefore aimed to investigate the expression of CaMKII in the dorsal horn in a rat model of early phase diabetes mellitus (DM) types 1 and 2. Sprague-Dawley rats were used. ⋯ No difference in IB4 expression was observed between the groups. These results suggest a potential role for CaMKII in diabetic neuropathy development. Inhibition of CaMKII signaling pathways should be further explored as a potential treatment target in painful diabetic neuropathy.