B-type natriuretic peptide is neither itch-specific nor functions upstream of the GRP-GRPR signaling pathway.
B-type natriuretic peptide is neither itch-specific nor functions upstream of the GRP-GRPR signaling pathway.
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DOI：
10.1186/1744-8069-10-4
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发表时间：
2014-01-18
期刊：
影响因子：
3.3
通讯作者：
Chen ZF
中科院分区：
文献类型：
--
作者：
Liu XY;Wan L;Huo FQ;Barry DM;Li H;Zhao ZQ;Chen ZF
Mishra和Hoon最近的一项研究将B型利钠肽（BNP）鉴定为瘙痒传递的重要肽，并提出BNP激活脊髓利钠肽受体-A（NPRA）表达神经元，其释放胃泌素释放肽（GRP）以激活GRP受体（GRPR）表达神经元，从而将瘙痒信息从外周传递到大脑（Science 340：968-971，2013）。这种新途径有效性的中心前提是背根神经节（DRG）神经元中缺乏GRP。为此，他们发现DRG神经元中的Grp mRNA要么不存在，要么几乎检测不到，并声称BNP而不是GRP是瘙痒感受器中的主要神经递质。他们表明，NPRA免疫染色与脊髓中的Grp-eGFP完全共定位，并测试了Nppb -/-小鼠的一些急性疼痛行为。他们声称BNP是一种瘙痒选择性肽，其充当包括用于瘙痒的GRP-GRPR级联的专用神经元通路的第一站。然而，我们的研究和其他研究沿着并不支持他们的说法。我们无法重现BNP和NPRA的免疫染色，如Mishra和Hoon所示。与此相反，我们能够检测Grp mRNA在DRG原位杂交和真实的时间RT-PCR。我们发现，GRP mRNA的表达模式与GRP蛋白在DRG中的表达模式相当。GRP-GRPR信号传导的药理学和遗传学阻断不会显著影响鞘内BNP诱导的抓挠行为。我们发现，BNP抑制炎性疼痛和吗啡镇痛。越来越多的证据表明，GRP是组胺受体介导非组胺依赖性瘙痒的关键神经递质。BNP-NPRA信号传导参与瘙痒和疼痛，并且在GRP-GRPR专用神经元通路的上游不起作用。BNP在瘙痒和疼痛中的作用部位及其与GRP的关系仍有待阐明。
A recent study by Mishra and Hoon identified B-type natriuretic peptide (BNP) as an important peptide for itch transmission and proposed that BNP activates spinal natriuretic peptide receptor-A (NPRA) expressing neurons, which release gastrin releasing peptide (GRP) to activate GRP receptor (GRPR) expressing neurons to relay itch information from the periphery to the brain (Science 340:968–971, 2013). A central premise for the validity of this novel pathway is the absence of GRP in the dorsal root ganglion (DRG) neurons. To this end, they showed that Grp mRNA in DRG neurons is either absent or barely detectable and claimed that BNP but not GRP is a major neurotransmitter for itch in pruriceptors. They showed that NPRA immunostaining is perfectly co-localized with Grp-eGFP in the spinal cord, and a few acute pain behaviors in Nppb -/- mice were tested. They claimed that BNP is an itch-selective peptide that acts as the first station of a dedicated neuronal pathway comprising a GRP-GRPR cascade for itch. However, our studies, along with the others, do not support their claims. We were unable to reproduce the immunostaining of BNP and NPRA as shown by Mishra and Hoon. By contrast, we were able to detect Grp mRNA in DRGs using in situ hybridization and real time RT-PCR. We show that the expression pattern of Grp mRNA is comparable to that of GRP protein in DRGs. Pharmacological and genetic blockade of GRP-GRPR signaling does not significantly affect intrathecal BNP-induced scratching behavior. We show that BNP inhibits inflammatory pain and morphine analgesia. Accumulating evidence demonstrates that GRP is a key neurotransmitter in pruriceptors for mediating histamine-independent itch. BNP-NPRA signaling is involved in both itch and pain and does not function upstream of the GRP-GRPR dedicated neuronal pathway. The site of BNP action in itch and pain and its relationship with GRP remain to be clarified.
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影响因子：
16.2
作者：
Wang X;Zhang J;Eberhart D;Urban R;Meda K;Solorzano C;Yamanaka H;Rice D;Basbaum AI
通讯作者：
Basbaum AI
影响因子：
2.5
作者：
FUXE, K;AGNATI, LF;CUELLO, AC
通讯作者：
CUELLO, AC
影响因子：
2.9
作者：
MARCOS, P;COVENAS, R;GONZALEZBARON, S
通讯作者：
GONZALEZBARON, S
DOI：
10.1126/science.1174868
发表时间：
2009-09-18
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Sun YG;Zhao ZQ;Meng XL;Yin J;Liu XY;Chen ZF
通讯作者：
Chen ZF
影响因子：
25
作者：
Han, Liang;Ma, Chao;Liu, Qin;Weng, Hao-Jui;Cui, Yiyuan;Tang, Zongxiang;Kim, Yushin;Nie, Hong;Qu, Lintao;Patel, Kush N.;Li, Zhe;McNeil, Benjamin;He, Shaoqiu;Guan, Yun;Xiao, Bo;LaMotte, Robert H.;Dong, Xinzhong
通讯作者：
Dong, Xinzhong