CONICET-Universidad de Buenos Aires, Instituto de Biología Celular y Neurociencia "Prof. Eduardo De Robertis" (IBCN), Buenos Aires, Argentina; Universidad de Buenos Aires, Facultad de Medicina, Departamento de Ciencias Fisiológicas, Buenos Aires, Argentina.
CONICET-Universidad de Buenos Aires, Instituto de Biología Celular y Neurociencia "Prof. Eduardo De Robertis" (IBCN), Buenos Aires, Argentina.
Pharmacol Biochem Behav. 2023 Jun;227-228:173594. doi: 10.1016/j.pbb.2023.173594. Epub 2023 Jun 27.
Emotional learning involves the association between sensory cues and rewarding or aversive stimuli, and this stored information can be recalled during memory retrieval. In this process, the medial prefrontal cortex (mPFC) plays an essential role. We have previously shown that the antagonism of α7 nicotinic acetylcholine receptors (nAChRs) by methyllycaconitine (MLA) in the mPFC blocked cue-induced cocaine memory retrieval. However, little is known about the involvement of prefrontal α7 nAChRs in the retrieval of aversive memories. Here, by using pharmacology and different behavioral tasks, we found that MLA did not affect aversive memory retrieval, indicating a differential effect of cholinergic prefrontal control of appetitive and aversive memories. Despite being shown that acetylcholine modulates dopamine release in the mPFC, it remains unknown if those modulatory systems act together to control reward-based behavior. We examined that question and found that dopamine type 1 receptor (D1R) activation prevented MLA-induced blockade of cocaine CPP retrieval. Our results suggest that α7 nAChRs and D1R signaling interact in the mPFC to modulate cocaine-associated memory retrieval.
情绪学习涉及感官线索与奖励或厌恶刺激之间的关联,并且这些存储的信息可以在记忆检索过程中被回忆起来。在这个过程中,内侧前额叶皮层(mPFC)起着至关重要的作用。我们之前已经表明,mPFC 中 α7 烟碱型乙酰胆碱受体(nAChRs)的拮抗剂甲基戊基aconitine(MLA)阻断了线索诱导的可卡因记忆检索。然而,对于前额叶 α7 nAChRs 在厌恶记忆检索中的参与知之甚少。在这里,通过使用药理学和不同的行为任务,我们发现 MLA 不会影响厌恶记忆的检索,表明胆碱能前额叶对食欲和厌恶记忆的控制具有不同的作用。尽管已经表明乙酰胆碱可以调节 mPFC 中的多巴胺释放,但仍不清楚这些调节系统是否共同作用以控制基于奖励的行为。我们研究了这个问题,发现多巴胺 D1 型受体(D1R)的激活可以防止 MLA 诱导的可卡因 CPP 记忆检索的阻断。我们的结果表明,mPFC 中的 α7 nAChRs 和 D1R 信号相互作用,调节与可卡因相关的记忆检索。