...
首页> 外文期刊>Journal of chemical neuroanatomy >G proteins in rat prefrontal cortex (PFC) are differentially activated as a function of oxygen status and PFC region.
【24h】

G proteins in rat prefrontal cortex (PFC) are differentially activated as a function of oxygen status and PFC region.

机译:大鼠前额叶皮层(PFC)中的G蛋白作为氧状态和PFC区域的函数而被不同地激活。

获取原文
获取原文并翻译 | 示例

摘要

This study tested the hypothesis that activation of guanine nucleotide binding (G) proteins in rat prefrontal cortex (PFC) is altered by hypoxia. G protein activation by the cholinergic agonist carbachol and the opioid agonist DAMGO was quantified using [(35)S]GTPgammaS autoradiography. G protein activation was expressed as nCi/g tissue in the PFC of 18 rats exposed for 14 consecutive days to sustained hypoxia (10% O(2)), intermittent hypoxia (10% and 21% O(2) alternating every 90 s), or room air (21% O(2)). Relative to basal levels of G protein activation, carbachol and DAMGO increased G protein activation by approximately 70% across all oxygen concentrations. Compared to the room air condition, sustained hypoxia caused a significant increase in G protein activation in frontal association (FrA) region of the PFC. Region-specific comparisons revealed that intermittent and sustained hypoxia caused greater DAMGO-stimulated G protein activation in the FrA than in the pre-limbic (PrL). The data show for the first time that hypoxia increased G protein activation in PFC. The results suggest the potential for hypoxia-induced enhancements in G protein activation to alter PFC function.
机译:这项研究检验了以下假设:缺氧会改变大鼠前额叶皮层(PFC)中鸟嘌呤核苷酸结合(G)蛋白的激活。胆碱能激动剂卡巴胆碱和阿片类激动剂DAMGO对G蛋白的激活作用用[(35)S] GTPgammaS放射自显影进行定量。 G蛋白激活被表示为连续14天暴露于持续缺氧(10%O(2)),间歇性缺氧(10%和21%O(2)每90 s交替进行14天的PFC中的nCi / g组织或室内空气(21%O(2))。相对于基础的G蛋白活化水平,在所有氧气浓度下,卡巴胆碱和DAMGO可使G蛋白活化增加约70%。与室内空气条件相比,持续的缺氧会导致PFC的额叶联想(FrA)区域中G蛋白激活的显着增加。特定区域的比较显示,间歇性和持续性缺氧导致FAM中DAMGO刺激的G蛋白活化程度高于前边缘(PrL)中。数据首次显示低氧增加了PFC中的G蛋白活化。结果表明,低氧诱导的G蛋白激活增强可能会改变PFC功能。

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