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苯二氮䓬类药物可逆转应激诱导的单胺氧化酶(MAO)A活性降低:外周苯二氮䓬受体的作用

The stress-induced reduction in monoamine oxidase (MAO) A activity is reversed by benzodiazepines: role of peripheral benzodiazepine receptors.

作者信息

Armando I, Lemoine A P, Segura E T, Barontini M B

机构信息

Centro de Investigaciones Endocrinologicas, CONICET, Hospital de Niños R. Gutierrez, Buenos Aires, Argentina.

出版信息

Cell Mol Neurobiol. 1993 Dec;13(6):593-600. doi: 10.1007/BF00711559.

DOI:10.1007/BF00711559
PMID:8194078
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11566934/
Abstract
  1. The effect of benzodiazepine pretreatment on the stress-induced decrease in MAO activity in rat tissues using footshock as stress model was investigated. 2. Animals were injected with vehicle, Lorazepam (1.25 mg/kg), or Clonazepam (0.5 mg/kg) 2 hr before or with PK 11195 (0.45 mg/kg) 2.5 hr before being subjected to one session of 10 inescapable footshocks or to a sham session. At the end of the session animals were sacrificed and MAO A and B activities in hearts and brains were determined. 3. Pretreatment of the animals with both Lorazepam and Clonazepam abolished the decrease induced by footshock in MAO A activity in brain. Pretreatment with Lorazepam but not with Clonazepam abolished the stress-induced decrease in MAO A in the heart. Pretreatment with PK 11195 before Lorazepam reversed its effects in the heart but not in the brain. Neither footshock nor any of the drugs used had any effect on heart and brain MAO B. 4. Our results suggest that in the heart but not in the brain, peripheral benzodiazepine receptors play a role in the regulation of MAO A activity under stress conditions.
摘要
  1. 以足部电击作为应激模型,研究了苯二氮䓬预处理对大鼠组织中应激诱导的单胺氧化酶(MAO)活性降低的影响。2. 在接受10次不可逃避的足部电击或假电击之前2小时,给动物注射赋形剂、劳拉西泮(1.25毫克/千克)或氯硝西泮(0.5毫克/千克),或者在接受电击前2.5小时注射PK 11195(0.45毫克/千克)。在实验结束时,处死动物并测定心脏和大脑中的MAO A和B活性。3. 用劳拉西泮和氯硝西泮对动物进行预处理,可消除足部电击诱导的大脑中MAO A活性的降低。用劳拉西泮而非氯硝西泮预处理可消除应激诱导的心脏中MAO A的降低。在劳拉西泮之前用PK 11195预处理可逆转其在心脏中的作用,但在大脑中则不然。足部电击及所用的任何药物均对心脏和大脑中的MAO B无任何影响。4. 我们的结果表明,在心脏而非大脑中,外周苯二氮䓬受体在应激条件下MAO A活性的调节中发挥作用。

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