VonVoigtlander P F, Losey E G
Res Commun Chem Pathol Pharmacol. 1976 Mar;13(3):389-400.
In pargyline or carbidopa pretreated mice, 6-hydroxydopa causes a depletion of brain norepinephrine. Several antidepressant compounds block the depletion after pargyline but not after carbidopa pretreatment. Similarly, p-chloromethamphetamine-induced depletion of brain 5-hydroxytryptamine is blocked by several antidepressants. Diazepam antagonizes the ability to imipramine to block the norepinephrine depletion induced by 6-hydroxydopa but not the 5-hydroxytryptamine depletion induced by p-chloromethamphetamine. Blockade of selective neurotoxic induced depletions of biogenic amines is a useful in vivo technique for determining the effects of drugs on the amine uptake systems. However, the results for compounds with mixed antidepressant/anxiolytic activity must be viewed with caution.
在使用帕吉林或卡比多巴预处理的小鼠中，6-羟基多巴胺会导致脑内去甲肾上腺素耗竭。几种抗抑郁化合物可阻断帕吉林预处理后的去甲肾上腺素耗竭，但对卡比多巴预处理后的耗竭无此作用。同样，对氯苯丙胺诱导的脑内5-羟色胺耗竭也可被几种抗抑郁药阻断。地西泮可拮抗丙咪嗪阻断6-羟基多巴胺诱导的去甲肾上腺素耗竭的能力，但不能拮抗其阻断对氯苯丙胺诱导的5-羟色胺耗竭的能力。阻断选择性神经毒性诱导的生物胺耗竭是一种用于确定药物对胺摄取系统影响的有用的体内技术。然而，对于具有抗抑郁/抗焦虑混合活性的化合物，其结果必须谨慎看待。
