Dubrovina N I, Il'yuchenok R Y
Institute of Physiology, Siberian Division, Russian Academy of Medical Sciences, Novosibirsk.
Neurosci Behav Physiol. 1998 May-Jun;28(3):294-8. doi: 10.1007/BF02462959.
Changes in the reactivating efficiency of blockade of components of the GABA-benzodiazepine-ionophore complex were analyzed in conditions of preliminary activation and inhibition of dopamine autoreceptors using (+)ZRRR and haloperidol respectively. A conditioned passive escape reflex was used, along with amnesia produced by detaining mice in the danger sector of a chamber immediately after imposition of a painful stimulus. Doses of bicuculline (1 mg/kg), picrotoxin (1 mg/kg), and flumazenil (10 mg/kg) given before testing restored performance of the conditioned response without altering the neurochemical background. Reductions and increases in dopaminergic activity during the training period prevented restoration of the conditioned passive escape response by blockade of GABAa and benzodiazepine receptors and chloride channels. It is suggested that the neurochemical mechanisms involved in restoring the damaged memory trace are based on the formation of te optimal balance in the activities of the various components of the GABA-benzodiazepine-ionophore complex and the dopaminergic system.
分别使用（+）ZRRR和氟哌啶醇在多巴胺自身受体的初步激活和抑制条件下，分析了GABA-苯二氮䓬-离子载体复合物各成分阻断的重新激活效率变化。使用了条件性被动逃避反射，以及在施加疼痛刺激后立即将小鼠关在实验箱危险区域所产生的失忆。在测试前给予荷包牡丹碱（1mg/kg）、印防己毒素（1mg/kg）和氟马西尼（10mg/kg）的剂量可恢复条件反应的表现，而不改变神经化学背景。训练期间多巴胺能活性的降低和增加阻止了通过阻断GABAa和苯二氮䓬受体以及氯离子通道来恢复条件性被动逃避反应。有人提出，恢复受损记忆痕迹所涉及的神经化学机制是基于在GABA-苯二氮䓬-离子载体复合物和多巴胺能系统的各种成分的活动中形成最佳平衡。
