期刊文献+

皮质酮快速升高大鼠脊髓背角神经元钙浓度

Rapid elevation of calcium concentration in rat dorsal spinal neurons by corticosterone
下载PDF
导出
摘要 目的:观察皮质酮(CORT)对培养的脊髓背角神经元Ca2+浓度([Ca2+]i)的调节作用及机制。方法:培养新生SD大鼠脊髓背角神经元,激光共聚焦显微镜检测神经元[Ca2+]i的变化。结果:CORT可快速升高培养的脊髓背角神经元[Ca2+]i,且呈现剂量依赖性(P<0.05);CORT诱导的神经元[Ca2+]i升高是以外钙内流为主(P<0.01);百日咳毒素(G蛋白活化阻断剂)可阻断CORT所致的脊髓背角神经元[Ca2+]i升高(P<0.01),而糖皮质激素受体拮抗剂RU38486对CORT的效应无抑制作用。结论:CORT通过非基因组途径快速增高培养的脊髓背角神经元[Ca2+]i。 Objective: To explore the modulatory effects of corticosterone (CORT) on the intracellular calcium concen- tration ( [Ca2+ ]i) in cultured rat dorsal spinal neurons and the relative mechanism. Methods:Neurons from neonatal SD rat spinal cord were cultured. Confocal laser scanning microscopy were employed to detect changes of [ Ca2+ ] i in cultured neurons. Results:CORT (0.1-10 μmo]/L) caused a rapid increase in [ Ca2+ ]i with a dose-dependent manner in cul- tured dorsal spinal neurons. The action of CORT on neuronal [ Ca2+] i was blocked by pertussis toxin ( a blocker of G protein activation, 100 ng/ml) , but was unaffected by RU38486 (glueocorticoid receptor antagonist, 10 μmol/L). Con- clusion : These observations suggest that CORT can rapidly increase [ Ca2+ ] i in cultured rat dorsal spinal neurons through a nongenomic mechanism.
出处 《神经解剖学杂志》 CAS CSCD 北大核心 2014年第1期40-44,共5页 Chinese Journal of Neuroanatomy
基金 国家自然科学基金(30960126 31000497) 遵义医学院重点学科建设项目(XZXK-20120702)
关键词 皮质酮 脊髓 神经元 corticosterone spinal cord neurons calcium
  • 相关文献

参考文献1

二级参考文献10

  • 1Nicholson K, Martelli M F. The problem of pain[J]. JHead Trauma Rehabil, 2004, 19(1): 2-9.
  • 2Wang S, Lim G, Zeng Q, et al. Expression of central glucocorticoid receptors after peripheral nerve injury contributes to neuropathic pain behaviors in mrs[J]. J Neurosci, 2004, 24 (39) : 8595-8605.
  • 3Bennett G J, Xie Y K. A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man[J]. Pain, 1988, 33(1): 87-107.
  • 4Kurpius D, Wilson N, Fuller L, et al. Early activation, motility, and homing of neonatal microglia to injured neurons does not require protein synthesis[ J]. Glia, 2006, 54(1) : 58-70.
  • 5Parris W C, Janicki P K, Johnson B, et al. Intrathecal ketorolac tromethamine produces analgesia after chronic con- striction injury of sciatic nerve in rat [ J ]. Can J Anaesth, 1996, 43(8): 867-870.
  • 6Mabuchi T, Kojima H, Abe T, et al. Membrane-associated prostaglandin E synthase-1 is required for neuropathic pain [J]. Neuroreport, 2004, 15(9): 1395-1398.
  • 7Vanegas H, Schaible H G. Prostaglandim and cycloxygenases in the spinal cord[J]. Prog Nettrobiol, 2001, 64(4): 327-363.
  • 8Freshwater J D, Svensson C I, Malmberg A B, etal. Elevated spinal cyclooxygenase and prostaglandin release during hyperalgesia in diabetic rats [ J ]. Diabetes, 2002, 51 (7) : 2249-2255.
  • 9Li S Q, Xing Y L, Chen W N, et al. Activation of NMDA receptor is associated with up-regulation of COX-2 expression in the spinal dorsal horn during nociceptive inputs in rats[ J]. Neurochem Res, 2009, 34(8): 1451-1463.
  • 10Wang S, Lim G, Zeng Q, et ol. Central glucocorticoid receptors modulate the expression and function of spinal NMDA receptors after peripheral nerve injury[J]. J Neurosci, 2005, 25(2) : 488-495.

共引文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部