Nucleus accumbens core acetylcholine receptors modulate the balance of flexible and inflexible cue-directed motivation.

Nucleus accumbens core acetylcholine receptors modulate the balance of flexible and inflexible cue-directed motivation.
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DOI:
10.1038/s41598-023-40439-4
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发表时间:
2023-08-17
期刊:
影响因子:
4.6
通讯作者:
--
中科院分区:
综合性期刊3区
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--
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符号追踪是一种条件反应,其中动物与奖励预测线索相互作用,因为这些线索具有激励价值或激励显著性。神经核的核心(NAc)已被牵连在介导的信号跟踪反应。此外,整个纹状体的乙酰胆碱(ACh)传输已被归因于激励动机和行为灵活性。在这里,我们证明了NAc ACh受体的灵活性的标志跟踪的作用。标志跟踪动物暴露于疏忽应急,其中大力标志跟踪惩罚奖励遗漏。动物们迅速调整了自己的行为,但它们以一种不那么积极的方式保持着跟踪信号的行为,这并没有取消奖励。在这种情况下的标志跟踪是持久的,但灵活的结构,NAC烟碱受体(nAChRs)的封锁导致了持久性的初始标志跟踪响应期间遗漏,随后一段时间的变化,标志跟踪的化妆,而阻断毒蕈碱受体(mAChRs)相反地增强了遗漏相关的发展新的标志跟踪行为。后来,一旦发生了遗漏学习,nAChR阻断会导致减少符号追踪和提高奖励导向行为。这些结果表明,NAc乙酰胆碱受体在维持学习模式的标志跟踪,与nAChRs有一个特殊的参与调节的结构的标志跟踪响应具有相反的作用。
Sign-tracking is a conditioned response where animals interact with reward-predictive cues due to the cues having motivational value, or incentive salience. The nucleus accumbens core (NAc) has been implicated in mediating the sign-tracking response. Additionally, acetylcholine (ACh) transmission throughout the striatum has been attributed to both incentive motivation and behavioral flexibility. Here, we demonstrate a role for NAc ACh receptors in the flexibility of sign-tracking. Sign-tracking animals were exposed to an omission contingency, in which vigorous sign-tracking was punished by reward omission. Animals rapidly adjusted their behavior, but they maintained sign-tracking in a less vigorous manner that did not cancel reward. Within this context of sign-tracking being persistent yet flexible in structure, blockade of NAc nicotinic receptors (nAChRs) led to a persistence in the initial sign-tracking response during omission followed by a period of change in the makeup of sign-tracking, whereas blockade of muscarinic receptors (mAChRs) oppositely enhanced the omission-related development of the new sign-tracking behaviors. Later, once omission learning had occurred, nAChR blockade uniquely led to reduced sign-tracking and elevated reward-directed behaviors instead. These results indicate that NAc ACh receptors have opposing roles in maintaining learned patterns of sign-tracking, with nAChRs having a special involvement in regulating the structure of the sign-tracking response.
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