Petty F, Jordan S, Kramer G L, Zukas P K, Wu J
Veterans Affairs Medical Center, University of Texas Southwestern Medical School, Dallas 75216, USA. PETTY.FREDERICK/DALLAS.VA.GOV
Neurochem Res. 1997 Sep;22(9):1101-4. doi: 10.1023/a:1027309117349.
In vivo microdialysis was used to determine the effect of diazepam, flumazenil and FG-7142 upon the biogenic amine response to acute and repeated swim stress in the medial prefrontal cortex of the rat. Acute swim stress increased norepinephrine levels, although dopamine and serotonin levels remained stable. Upon re-exposure to swim stress twenty-four hours later, sustained increases (200-300% of baseline) in all three biogenic amines were detected. This enhanced response to re-stress was not seen in rats pretreated with either a benzodiazepine: agonist (diazepam, 2 mg/kg), an antagonist (flumazenil, 10 mg/kg), or an inverse agonist (FG-7142, 10 mg/kg) given prior to the first swim stress. Therefore, the sensitization of biogenic amine response to re-stress may be prevented by compounds which differ in their activity at the benzodiazepine receptor.
采用体内微透析技术，以确定地西泮、氟马西尼和FG - 7142对大鼠内侧前额叶皮质中生物胺对急性和重复游泳应激反应的影响。急性游泳应激使去甲肾上腺素水平升高，而多巴胺和5-羟色胺水平保持稳定。在24小时后再次暴露于游泳应激时，检测到所有三种生物胺均持续升高（为基线水平的200 - 300%）。在首次游泳应激前预先给予苯二氮䓬类激动剂（地西泮，2mg/kg）、拮抗剂（氟马西尼，10mg/kg）或反向激动剂（FG - 7142，10mg/kg）的大鼠中，未观察到这种对再应激的增强反应。因此，苯二氮䓬受体活性不同的化合物可能会阻止生物胺对再应激反应的致敏作用。
