Involvement of insular muscarinic cholinergic receptors in morphine-induced conditioned place preference in rats

Involvement of insular muscarinic cholinergic receptors in morphine-induced conditioned place preference in rats
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岛叶毒蕈碱胆碱能受体参与吗啡诱导的大鼠条件性位置偏爱

DOI:
10.1007/s00213-014-3550-1
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发表时间:
2014-04
期刊:
影响因子:
3.4
通讯作者:
Zhai, Haifeng
Zhai, Haifeng
中科院分区:
医学3区
文献类型:
--
作者:
Liu, Yu;Huang, Xinjie;Chen, Lei;Zhai, Haifeng

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药物成瘾代表了一种病理性的神经过程的篡夺,涉及学习和记忆。恢复与毒品有关的记忆会导致对毒品的渴望和复发。目的探讨岛叶毒蕈碱型乙酰胆碱受体(mAChRs)在药物记忆过程中的作用。所有大鼠首先用吗啡训练以建立CPP。这些大鼠的亚组用于上下文线索诱导的CPP恢复。其他亚组的大鼠进行消退的CPP,和5 m/kg吗啡用于引发诱导的CPP恢复。在CPP测试之前,将mAChR拮抗剂或激动剂微量注射到海马中,以评估其对CPP表达的影响。结果非选择性mAChR拮抗剂东莨菪碱和M1拮抗剂哌仑西平在上下文提示和引发诱导的CPP恢复中均显著抑制CPP表达; M1受体激动剂MCN-A-343和M4受体拮抗剂托吡卡胺可增强CPP表达。M4激动剂LY 2033298抑制CPP表达。M2受体拮抗剂methoctramine和M3受体拮抗剂4-DAMP对CPP表达无影响。M1和M4 mAChRs的作用是矛盾的,M1激活和M4抑制可减弱药物记忆的表达,而M1抑制和M4激活可增强药物记忆的表达。
RationaleDrug addiction represents a pathological usurpation of neural processes involved in learning and memory. Retrieval of drug-related memories can result in drug craving and relapse. Recently, the insula was identified as part of the neuronal circuit responsible for the processing of drug memory; however, its precise role remains unclear.ObjectiveTo investigate the involvement of insular muscarinic acetylcholine receptors (mAChRs) in the processing of drug memory.MethodThe morphine-induced conditioned place preference (CPP) was used to assess drug memory. All rats were first trained with morphine to establish the CPP. Sub-groups of these rats were used for contextual cue-induced CPP reinstatement. Other sub-groups of rats underwent extinction of the CPP, and 5 m/kg morphine was used for priming-induced CPP reinstatement. Microinjection of mAChR antagonists or agonists into the insula was performed prior to the CPP tests in order to evaluate their effect on CPP expression.ResultsInsular microinjections of the nonselective mAChR antagonist, scopolamine, and the M1antagonist, pirenzepine, significantly inhibited CPP expression in both contextual cue- and priming-induced CPP reinstatement; the M1agonist, MCN-A-343, and the M4antagonist, tropicamide, enhanced CPP expression. The M4agonist, LY2033298, inhibited CPP expression. The M2antagonist, methoctramine, and M3antagonist, 4-DAMP, had no effect on CPP expression.ConclusionOur results demonstrate that insular mAChRs play a role in the processing of drug memory. M1and M4mAChRs work paradoxically; M1activation and M4inhibition attenuate the expression of drug memory, while M1inhibition and M4activation augment the expression of drug memory.
DOI: 10.32388/g282ih
发表时间: 2020-02
期刊: Substance Use Disorders
影响因子: --
作者:
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通讯作者: A. Ansari;David N. Osser
DOI: 10.1016/j.tins.2008.09.009
发表时间: 2009-01
影响因子: 15.9
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DOI: 10.1016/j.brainresbull.2008.02.003
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影响因子: 3.8
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通讯作者: B. Esmaeili;Zahra Basseda;A. Dehpour