每周论文更新----21 Oct 2016
每周论文更新----21 Oct 2016周伯通博士 本周推送三篇文章，分别来自Nature Neuroscience、Nature Communications和Cell Reports杂志。文章的题目分别为："TRPA1 mediates sensation ofthe rate of temperature change in Drosophila larvae"、“Glucocorticoidregulation of ATP release from spinal astrocytes underlies diurnal exacerbation of neuropathic mechanical allodynia"和“HMGB1 Activates Proinflammatory Signaling via TLR5 Leading to Allodynia”。 第一篇TRPA1 mediates sensation ofthe rate of temperature change in Drosophila larvaeTRPA1介导果蝇幼虫感觉环境温度的快慢变化Luo J, Shen WL, Montell CNat Neurosci. 2016 Oct 17PMID: 27749829AbstractAvoidance of noxious ambient heat is crucialfor survival. A well-known phenomenon is that animals are sensitive tothe rate of temperature change. However, the cellular andmolecular underpinnings through which animals sense and respond much morevigorously to fast temperature changes are unknown.Using Drosophila larvae, we found that nociceptive rolling behaviorwas triggered at lower temperatures and at higher frequencies whenthe temperature increased rapidly. We identified neurons in the brainthat were sensitive to the speed of the temperature increase ratherthan just to the absolute temperature. These cellular and behavioralresponses depended on the TRPA1 channel, whose activity responded tothe rate of temperature increase. We proposethat larvae use low-threshold sensors in the brain to monitorrapid temperature increases as a protective alert signal to triggerrolling behaviors, allowing fast escape before the temperature of thebrain rises to dangerous levels. 全文链接:http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.4416.html 第二篇Glucocorticoid regulation of ATP release fromspinal astrocytes underlies diurnal exacerbation ofneuropathic mechanical allodynia糖皮质激素通过调控脊髓星形细胞ATP的释放来介导神经病理性疼痛机械性痛觉异常的日益增强Koyanagi S, Kusunose N, Taniguchi M, AkamineT, Kanado Y, Ozono Y, Masuda T, Kohro Y, Matsunaga N, Tsuda M, Salter MW, InoueK, Ohdo S.Nat Commun. 2016 Oct 14PMID: 27739425AbstractDiurnal variations in painhypersensitivity are common in chronic pain disorders, but the underlyingmechanisms are enigmatic. Here, we report that mechanical painhypersensitivity in sciatic nerve-injured mice showspronounced diurnal alterations, which critically dependon diurnal variations in glucocorticoids from the adrenal glands. Diurnal enhancementof pain hypersensitivity is mediated by glucocorticoid-induced enhancementof the extracellular release of ATP inthe spinal cord, which stimulates purinergic receptors on microgliain the dorsal horn. We identify serum- and glucocorticoid-induciblekinase-1 (SGK-1) as the key molecule responsible forthe glucocorticoid-enhanced release of ATP from astrocytes.SGK-1 protein levels in spinal astrocytes are increased inresponse to glucocorticoid stimuli andenhanced ATP release by opening the pannexin-1 hemichannels. Ourfindings reveal an unappreciated circadian machinery affecting painhypersensitivity caused by peripheral nerve injury, thus opening up novelapproaches to the management of chronic pain.全文链接：http://dx.doi.org/10.1038/ncomms13102 第三篇HMGB1 Activates Proinflammatory Signaling via TLR5 Leading to Allodynia.HMGB1激活TLR5通过促炎症信号介导了机械痛觉异常的产生Das N, Dewan V, Grace PM, Gunn RJ, Tamura R,Tzarum N, Watkins LR, Wilson IA, Yin H.Cell Rep. 2016 Oct 18PMID: 27760316 AbstractInfectious and sterile inflammatory diseasesare correlated with increased levels of high mobility group box 1 (HMGB1) intissues and serum. Extracellular HMGB1 is known to activate Toll-likereceptors (TLRs) 2 and 4 and RAGE (receptor for advanced glycation endproducts)in inflammatory conditions. Here, we find that TLR5 is alsoan HMGB1 receptor that was previously overlooked due to lack offunctional expression in the cell lines usually used for studyingTLR signaling. HMGB1 binding to TLR5 initiates theactivation of NF-κB signaling pathway in a MyD88-dependent manner,resulting in proinflammatory cytokine production and pain enhancementin vivo. Biophysical and in vitro results highlight an essentialrole for the C-terminal tail region of HMGB1 in facilitatinginteractions with TLR5. These results suggestthat HMGB1-modulated TLR5 signaling is responsible for painhypersensitivity.
全文链接：http://www.cell.com/cell-reports/pdf/S2211-1247(16)31332-8.pdf 欢迎长按二维码关注“疼痛研究论坛”。
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