Mason S T, Fibiger H C
Pharmacol Biochem Behav. 1979 Mar;10(3):373-80. doi: 10.1016/0091-3057(79)90200-4.
Injection of 6-hydroxydopamine into the mesencephalon of the rat has been found to cause resistance to extinction on continuously reinforced schedules. The neurochemical basis of this effect was investigated by using another concentration of 6-hydroxydopamine and by another position of injection. Severe depletion of forebrain noradrenaline was found after these injections with no change in dopamine, serotonin, cholinergic or GABAergic parameters in any brain area measured. The noradrenergic nature of the effect was further shown by the reversal fo the usual behavioural effect following pretreatment with a noradrenaline uptake inhibitor (desimipramine, 25 mg/kg 30 min prior to intracerebral injection of 6-hydroxydopamine). This rules out non-specific damage caused by the 6-hydroxydopamine as the neurochemical basis of the dorsal bundle extinction effect. Failure to find resistance to extinction after either kainic acid or 5-7 dihydroxytryptamine injection seems also to exclude respectively cell body loss at the injection site or damage to serotonergic systems. It is concluded that the dorsal bundle extinction effect is noradrenergic in nature.
已发现向大鼠中脑注射6-羟基多巴胺会导致在持续强化程序中对消退产生抗性。通过使用另一种浓度的6-羟基多巴胺和另一个注射位置来研究这种效应的神经化学基础。这些注射后发现前脑去甲肾上腺素严重耗竭,而在所测量的任何脑区中多巴胺、5-羟色胺、胆碱能或γ-氨基丁酸能参数均无变化。在用去甲肾上腺素摄取抑制剂(地昔帕明,在脑内注射6-羟基多巴胺前30分钟给予25mg/kg)预处理后,通常的行为效应发生逆转,这进一步表明了该效应的去甲肾上腺素能性质。这排除了6-羟基多巴胺引起的非特异性损伤作为背束消退效应的神经化学基础。注射 kainic 酸或5,7-二羟基色胺后未发现对消退的抗性,这似乎也分别排除了注射部位的细胞体损失或5-羟色胺能系统的损伤。得出的结论是,背束消退效应本质上是去甲肾上腺素能的。