Expression of vesicular glutamate transporters in transient receptor potential melastatin 8 (TRPM8)-positive dental afferents in the mouse.

Expression of vesicular glutamate transporters in transient receptor potential melastatin 8 (TRPM8)-positive dental afferents in the mouse.
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小鼠瞬时受体电位美塑蛋白 8 (TRPM8) 阳性牙齿传入细胞中囊泡谷氨酸转运蛋白的表达。

DOI:
10.1016/j.neuroscience.2015.07.013
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发表时间:
2015-09-10
期刊:
影响因子:
3.3
通讯作者:
Bae YC
Bae YC
中科院分区:
医学3区
文献类型:
--
作者:
Kim YS;Kim TH;McKemy DD;Bae YC

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瞬时受体电位melastatin 8(TRPM 8)在冷刺激和冷刺激下被激活,在冷刺激引起的急性疼痛和疼痛超敏反应中起重要作用。为了帮助理解在正常和病理条件下TRPM 8介导的冷感知的机制,我们在TRPM 8阳性(+)神经元中表达基因编码的轴突示踪剂的小鼠中使用光镜免疫组织化学和Western印迹分析。我们研究了TRPM 8和囊泡谷氨酸转运蛋白1(VGLUT 1)和VGLUT 2在三叉神经节(TG)和牙髓诱导牙髓炎症前后的共表达。TG中的许多TRPM 8+神经元和牙髓轴突表达VGLUT 2,而没有表达VGLUT 1。TRPM 8+轴突在牙髓角和周围牙髓中密集,也经常在牙本质小管中观察到。牙髓炎症后,VGLUT 2+和VGLUT 2 +/TRPM 8+神经元的比例显著增加,而TRPM 8+神经元的比例保持不变。我们的研究结果表明,在TRPM 8+神经元中存在VGLUT 2(而不是VGLUT 1)介导的谷氨酸信号传导,可能是牙髓炎症后冷诱导的急性疼痛和对冷的超敏反应的基础。
Transient receptor potential melastatin 8 (TRPM8) is activated by innocuous cool and noxious cold and plays a crucial role in cold-induced acute pain and pain hypersensitivity. To help understand the mechanism of TRPM8-mediated cold perception under normal and pathologic conditions, we used light microscopic immunohistochemistry and Western blot analysis in mice expressing a genetically encoded axonal tracer in TRPM8-positive (+) neurons. We investigated the coexpression of TRPM8 and vesicular glutamate transporter 1 (VGLUT1) and VGLUT2 in the trigeminal ganglion (TG) and the dental pulp before and after inducing pulpal inflammation. Many TRPM8+ neurons in the TG and axons in the dental pulp expressed VGLUT2, while none expressed VGLUT1. TRPM8+ axons were dense in the pulp horn and peripheral pulp and also frequently observed in the dentinal tubules. Following pulpal inflammation, the proportion of VGLUT2+ and of VGLUT2+/TRPM8+ neurons increased significantly, whereas that of TRPM8+ neurons remained unchanged. Our findings suggest the existence of VGLUT2 (but not VGLUT1)-mediated glutamate signaling in TRPM8+ neurons possibly underlying the cold-induced acute pain and hypersensitivity to cold following pulpal inflammation.