Behavioral Pharmacology Group, Laboratory of Animal Morphology and Pathology, State University of North Fluminense Darcy Ribeiro, Avenida Alberto Lamego, 2000, Campos dos Goytacazes, 28013-602, RJ, Brazil.
SUNY Upstate Medical University, 800 Irving Avenue, Syracuse, NY 13210, USA.
Behav Brain Res. 2013 Jan 1;236(1):244-250. doi: 10.1016/j.bbr.2012.06.025. Epub 2012 Jun 30.
Re-exposure to conditioned drug stimuli triggers re-consolidation processes. In the present study post-trial apomorphine treatments were administered in order to interact with the re-consolidation of an apomorphine conditioned/sensitized locomotor response. A low (0.05 mg/kg) and a high (2.0mg/kg) dose were used to inhibit or to enhance dopamine activity, respectively. Initially, groups received 5 daily apomorphine (2.0mg/kg)/vehicle treatments either paired or unpaired to open-field placement. The paired treatments generated a progressive locomotor response. Subsequently, all groups received a 5 min non-drug test for conditioning and a conditioned locomotor response was observed in the paired group. The groups received another apomorphine (2.0mg/kg)/vehicle treatment as a re-induction treatment. At this stage the post-trial protocol was initiated. One set of paired, unpaired and vehicle groups were given a low dose of apomorphine (0.05 mg/kg) post-trial; another set received a high dose of apomorphine (2.0mg/kg) post-trial. The remaining group set received vehicle post-trial. The low dose post-trial treatment eliminated the conditioned and sensitized locomotor response and the high dose post-trial treatment enhanced the conditioned and sensitized locomotor response. The efficacy of the post-trial apomorphine treatments to modify the conditioned and the sensitized response after a brief non-drug exposure to test cues supports the proposition that exteroceptive cues control conditioning and sensitization and that the interoceptive drug cues make little or no associational contribution to apomorphine conditioning and sensitization. In addition, the findings point to the importance of dopamine activation in both the acquisition and re-consolidation of conditioning processes.
重新暴露于条件性药物刺激会引发再巩固过程。在本研究中，给予试验后阿扑吗啡处理，以与阿扑吗啡条件/敏化运动反应的再巩固相互作用。使用低（0.05mg/kg）和高（2.0mg/kg）剂量分别抑制或增强多巴胺活性。最初，各组接受 5 天每日阿扑吗啡（2.0mg/kg）/载体处理，与开放场放置配对或不配对。配对处理产生了渐进的运动反应。随后，所有组都接受了 5 分钟的非药物测试以进行条件化，并且在配对组中观察到了条件化的运动反应。各组接受了另一次阿扑吗啡（2.0mg/kg）/载体处理作为再诱导处理。在这个阶段，开始了试验后方案。一组配对、不配对和载体组在试验后给予低剂量阿扑吗啡（0.05mg/kg）；另一组在试验后给予高剂量阿扑吗啡（2.0mg/kg）。其余组在试验后给予载体。试验后低剂量处理消除了条件化和敏化运动反应，而高剂量处理增强了条件化和敏化运动反应。在短暂的非药物暴露于测试线索后，试验后阿扑吗啡处理对改变条件化和敏化反应的有效性支持了以下观点：外感受线索控制条件化和敏化，而内感受药物线索对阿扑吗啡条件化和敏化几乎没有或没有关联贡献。此外，这些发现指出了多巴胺激活在条件化过程的获得和再巩固中的重要性。
