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

应激诱导的单胺氧化酶(MAO)A活性降低可被苯二氮卓类药物逆转:外周苯二氮卓受体的作用

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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.

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