Dubrovina N I, Zinov'eva D V
Zh Vyssh Nerv Deiat Im I P Pavlova. 2008 Sep-Oct;58(5):605-10.
Selectivity of training and extinction of passive avoidance response caused by pharmacological influences on D1 and D2 dopamine receptors in intact mice and mice in depressive-like state was shown. Training was impaired only by administration of D2 receptor antagonist sulpiride and did not depend on the initial functional condition of mice. In intact mice, activation of D2 receptors by quinpirole evoked deficiency of extinction, i.e., impairment of the capability of new inhibitory training under conditions of disappearance of the expected punishment. In mice with reaction of "behavioral despair" characterized by a delay of extinction, activation of D1 receptors by SKF38393 normalized this process (as distinct from the inefficiency of D2 agonist). The positive effect of acceleration of fear memory extinction was revealed also under conditions of blockade of D1 and D2 dopamine receptors.
研究表明了在完整小鼠和处于类抑郁状态小鼠中，药理学作用于D1和D2多巴胺受体对被动回避反应训练的选择性以及消退情况。只有给予D2受体拮抗剂舒必利时训练才会受损，且这并不取决于小鼠的初始功能状态。在完整小鼠中，喹吡罗激活D2受体会引发消退缺陷，即在预期惩罚消失的情况下新的抑制性训练能力受损。在具有“行为绝望”反应（表现为消退延迟）的小鼠中，SKF38393激活D1受体使这一过程正常化（这与D2激动剂无效不同）。在D1和D2多巴胺受体被阻断的情况下，也发现了加速恐惧记忆消退的积极作用。
