...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Spinal heat shock protein (70) expression: effect of spinal ischemia, hyperthermia (42 degrees C)/hypothermia (27 degrees C), NMDA receptor activation and potassium evoked depolarization on the induction.
【24h】

Spinal heat shock protein (70) expression: effect of spinal ischemia, hyperthermia (42 degrees C)/hypothermia (27 degrees C), NMDA receptor activation and potassium evoked depolarization on the induction.

机译：脊髓热休克蛋白（70）表达：脊髓缺血，热疗（42摄氏度）/体温过低（27摄氏度），NMDA受体激活和钾诱发的去极化对诱导的影响。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

The present study shows that anoxic neuronal depolarization or NMDA receptor activation are potent stimuli for inducing spinal neuronal heat shock protein 70 (Hsp70). Spinal hyperthermia, despite its significant glutamate releasing effect, induced only glial Hsp70 upregulation. No significant increase in spinal Hsp70 expression after potassium depolarization was seen. Transient spinal ischemia (6 min) was induced by the inflation of a 2F Fogarty catheter placed into descending thoracic aorta during concurrent hypotension (40 mmHg). To determine the onset of anoxic depolarization extracellular concentration of K+ was measured in the lumbar dorsal horn using a microelectrode. Spinal hyperthermia (42 degrees C) or hypothermia (27 degrees C) was induced using a heat exchanger placed in the paravertebral subcutaneous space overlying Th5-S4 spinal segments. To measure extracellular concentration of glutamate during hyperthermia a loop dialysis catheter was implanted into lumbar intrathecal space. Receptor specific (NMDA, 3 microg) or non-specific (KCl, 10 microl, 1M) neuronal depolarization was induced using previously implanted intrathecal catheters. After ischemia, temperature manipulations or drug injections animals survived for 4 or 24h. Animals were then terminally anesthetized and perfusion fixed for Hsp70 immunohistochemistry. After spinal ischemia or NMDA administration a neuronal Hsp70 expression was seen at 24h. After spinal hyperthermia only glial expression was seen at 4h. Hyperthermia significantly increased CSF glutamate concentration, however, MK-801 (a non-competitive NMDA receptor antagonist) pretreatment failed to block Hsp70 expression. After hypothermia or potassium depolarization only minimal or no Hsp70 expression was seen in glial cells. Exposure of neuronal tissue to a specific stimuli may lead to intervals of increased resistance to subsequent neurotoxic/ischemic insult. The intervening biochemistry of this protection has been attributed to a family of molecules referred to as HSP. In the present study, we demonstrate that short-lasting anoxic depolarization or activation of NMDA receptor are the most potent stimuli for spinal neuronal Hsp70 induction. This effect corresponds with the observed ischemic tolerance state induced by short-lasting preconditioning spinal ischemia.
机译：本研究表明，缺氧神经元去极化或NMDA受体激活是诱导脊髓神经元热休克蛋白70（Hsp70）的有效刺激。脊髓热疗尽管具有显着的谷氨酸释放作用，但仅诱导神经胶质Hsp70上调。钾去极化后，脊髓Hsp70表达未见明显增加。在并发低血压（40 mmHg）期间，将2F Fogarty导管置入胸主动脉下降，可引起短暂性脊髓缺血（6分钟）。为了确定缺氧去极化的发生，使用微电极在腰背角中测量了K +的细胞外浓度。使用放置在Th5-S4脊柱节段上方的椎旁皮下空间中的换热器诱导脊髓热疗（42摄氏度）或体温过低（27摄氏度）。为了测量热疗期间谷氨酸的细胞外浓度，将环形透析导管植入腰椎鞘内空间。使用先前植入的鞘内导管诱导受体特异性（NMDA，3微克）或非特异性（KCl，10微升，1M）神经元去极化。缺血，温度控制或药物注射后，动物存活4或24小时。然后将动物终末麻醉并灌注以进行Hsp70免疫组织化学。脊髓缺血或NMDA给药后，在24小时观察到神经元Hsp70表达。脊柱热疗后4小时仅见神经胶质表达。热疗显着增加了CSF谷氨酸的浓度，但是，MK-801（一种非竞争性NMDA受体拮抗剂）预处理未能阻止Hsp70的表达。体温过低或钾去极化后，在胶质细胞中仅观察到极少或没有Hsp70表达。将神经元组织暴露于特定刺激下可能会导致对随后的神经毒性/缺血性损伤的抵抗力增加。这种保护作用的介入生物化学已经归因于称为HSP的分子家族。在本研究中，我们证明了短时的缺氧去极化或NMDA受体的激活是脊髓神经元Hsp70诱导最有效的刺激。这种作用与观察到的由短期预适应性脊髓缺血引起的缺血耐受状态相对应。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号