TRESK contributes to pain threshold changes by mediating apoptosis via MAPK pathway in the spinal cord
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- 作者：Jun Zhoua ; zhoujun7843@126.com" class="auth_mail" title="E-mail the corresponding author ; Wenjing Lina ; Hongtao Chenb ; Youling Fanc ; Chengxiang Yanga
- 关键词：ANOVA ; analysis of variance ; DRG ; dorsal root ganglia ; ERK ; extracellular signal-regulated kinase ; IL ; interleukin ; JNK ; c-Jun N-terminal kinase ; K2P ; two-pore domain K+ ; MAPK ; mitogen-activated protein kinase ; MCP-1 ; monocyte chemotactic protein-1 ; MIP-2 ; macrophage inflammatory protein-2 ; MWT ; mechanical withdrawal thresholds ; NP ; neuropathic pain ; NS ; normal saline ; PCR ; polymerase chain reaction ; SEM ; standard error of mean ; SNI ; spared nerve injury ; TRESK ; the TWIK-related spinal cord K+ ; T
- 刊名：Neuroscience
- 出版年：2016
- 出版时间：17 December 2016
- 年：2016
- 卷：339
- 期：Complete
- 页码：622-633
- 全文大小：3580 K
文摘
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Upregulation of TRESK alleviates hyperalgesia and neurons apoptosis induced by NP.
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Upregulation of TRESK inhibits activation of caspase 3 and upregulation of Bax.
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Upregulation of TRESK reduces inflammatory factors production in spinal cord.
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Downregulation of TRESK can induce to hyperalgesia in normal rats.
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TRESK contributes to pain threshold changes mediated by ERK and p38 MAPK.