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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蛋白被差异激活作为氧状态和PFC区域的函数

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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 [35S]GTPγS autoradiography. G proteins were expressed as nCi/g tissue in the PFC of 18 rats exposed for 14 consecutive days to sustained hypoxia (10 % O2), intermittent hypoxia (10 % and 21 % O2 alternating every 90 s), or room air (21 % O2). 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 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。用[ 35 S]GTPγS放射自显影术定量胆碱能激动剂卡巴胆碱和阿片类激动剂DAMGO对G蛋白的活化作用。 G蛋白表示为连续暴露14天连续缺氧(10%O2),间歇性缺氧(10%和21%O2每90秒交替出现一次)或室内空气(21%)的18只大鼠的PFC中的nCi / g组织O2)。相对于基础水平的G蛋白活化,在所有氧气浓度下,卡巴胆碱和DAMGO可使G蛋白活化提高约70%。与室内空气条件相比,持续的缺氧会导致PFC的额叶缔合(FrA)区域G蛋白活化显着增加。特定区域的比较显示,间歇性和持续性缺氧导致FrA中DAMGO刺激的G蛋白活化大于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。

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