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吸入二氧化碳、应激和致焦虑药物会降低大鼠脑中GABAA受体复合物的功能。

Carbon dioxide inhalation, stress and anxiogenic drugs reduce the function of GABAA receptor complex in the rat brain.

作者信息

Concas A, Sanna E, Cuccheddu T, Mascia M P, Santoro G, Maciocco E, Biggio G

机构信息

Department of Experimental Biology, University of Cagliari, Italy.

出版信息

Prog Neuropsychopharmacol Biol Psychiatry. 1993 Jul;17(4):651-61. doi: 10.1016/0278-5846(93)90012-h.

Abstract
  1. The effect of different stressful stimuli on the function of the GABAA-ionophore receptor complex was evaluated by measuring the binding of 35S-TBPS to the chloride channel associated recognition sites. 2. Foot-shock stress enhanced 35S-TBPS binding in membrane preparation from rat cerebral cortex. The effect of foot-shock on 35S-TBPS binding was mimicked by the anxiogenic and proconvulsant beta-carboline FG 7142 and antagonized by anxiolytic benzodiazepines and by the novel anxiolytic and anticonvulsant beta-carboline, abecarnil. 3. A brief exposure of rats to CO2 inhalation produced, like foot-shock and FG 7142, a marked increase of 35S-TBPS binding in the cerebral cortex, cerebellum and hippocampus. The effect of CO2 inhalation was maximal 10 min after treatment and return to control value in 2 hours. Previous administration of anxiolytic drugs (alprazolam and abecarnil) completely prevented the CO2 inhalation-induced increase of 35S-TBPS binding. 4. All together these data strongly suggest that carbon dioxide inhalation, like stress and anxiogenic drugs, decreases the function of the GABAA receptor complex.
摘要
  1. 通过测量³⁵S - TBPS与氯离子通道相关识别位点的结合,评估不同应激刺激对GABAA离子载体受体复合物功能的影响。2. 足部电击应激增强了大鼠大脑皮质膜制备物中³⁵S - TBPS的结合。致焦虑和促惊厥的β - 咔啉FG 7142模拟了足部电击对³⁵S - TBPS结合的影响,而抗焦虑的苯二氮䓬类药物以及新型抗焦虑和抗惊厥的β - 咔啉阿贝卡尼则拮抗了这种影响。3. 大鼠短暂吸入二氧化碳后,与足部电击和FG 7142一样,大脑皮质、小脑和海马体中³⁵S - TBPS的结合显著增加。吸入二氧化碳的影响在处理后10分钟达到最大,并在2小时内恢复到对照值。预先给予抗焦虑药物(阿普唑仑和阿贝卡尼)可完全阻止吸入二氧化碳引起的³⁵S - TBPS结合增加。4. 所有这些数据有力地表明,吸入二氧化碳与应激和致焦虑药物一样,会降低GABAA受体复合物的功能。

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