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脑特异性神经锌指转录因子2b（NZF-2b/7ZFMyt1）抑制大鼠可卡因自我给药行为。

The Brain-Specific Neural Zinc Finger Transcription Factor 2b (NZF-2b/7ZFMyt1) Suppresses Cocaine Self-Administration in Rats.

作者信息

Chandrasekar Vijay, Dreyer Jean-Luc

机构信息

Division of Biochemistry, Department of Medicine, University of Fribourg Fribourg, Switzerland.

出版信息

Front Behav Neurosci. 2010 Apr 5;4:14. doi: 10.3389/fnbeh.2010.00014. eCollection 2010.

DOI:10.3389/fnbeh.2010.00014
PMID:20407577
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2854526/
Abstract

Brain-specific neural-zinc-finger transcription factor-2b (NZF2b/7ZFMyt1) is induced in the mesolimbic dopaminergic region after chronic cocaine exposure and lentiviral-mediated expression of NZF2b/7ZFMyt1 in the nucleus accumbens results in decreased locomotor activity (Chandrasekar and Dreyer, 2010). In this study the role of NZF2b/7ZFMyt1 in active cocaine seeking and of its interaction with histone deacetylase on the altered behavior has been observed. Localized expression of NZF2b/7ZFMyt1 in the nucleus accumbens resulted in attenuated cocaine self-administration, whereas silencing this transcription factor with lentiviruses expressing siRNAs increased the animal's motivation to self-infuse cocaine. Low doses of sodium butyrate, a potent inhibitor of histone deacetylase, were sufficient to reverse the NZF2b/7ZFMyt1-mediated decrease in cocaine self-administration. NZF2b/7ZFMyt1 expression resulted in strong induction of transcription factors REST1 and NAC1 and of the dopamine D2 receptor, with concomitant inhibition of BDNF and its receptor TrkB. We show that NZF2b/7ZFMyt1 colocalizes with histone deacetylase-2 (HDAC2), probably overcoming the suppression of transcriptional activity caused by Lingo1. These findings show that molecular adaptations mediated by NZF2b/7ZFMyt1 expression possibly lead to decreased responsiveness to the reinforcing properties of cocaine and play a prominent role in affecting the behavioral changes induced by the drug.

摘要

脑特异性神经锌指转录因子2b（NZF2b/7ZFMyt1）在长期接触可卡因后于中脑边缘多巴胺能区域被诱导，并且在伏隔核中通过慢病毒介导的NZF2b/7ZFMyt1表达会导致运动活性降低（钱德拉塞卡尔和德雷尔，2010年）。在本研究中，观察到了NZF2b/7ZFMyt1在主动寻求可卡因行为中的作用及其与组蛋白去乙酰化酶在行为改变方面的相互作用。NZF2b/7ZFMyt1在伏隔核中的局部表达导致可卡因自我给药减弱，而用表达小干扰RNA的慢病毒使该转录因子沉默则增加了动物自我注射可卡因的动机。低剂量的丁酸钠（一种有效的组蛋白去乙酰化酶抑制剂）足以逆转NZF2b/7ZFMyt1介导的可卡因自我给药减少。NZF2b/7ZFMyt1的表达导致转录因子REST1和NAC1以及多巴胺D2受体的强烈诱导，同时抑制脑源性神经营养因子（BDNF）及其受体TrkB。我们发现NZF2b/7ZFMyt1与组蛋白去乙酰化酶2（HDAC2）共定位，可能克服了由Lingo1引起的转录活性抑制。这些发现表明，由NZF2b/7ZFMyt1表达介导的分子适应性变化可能导致对可卡因强化特性的反应性降低，并在影响药物诱导的行为变化中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/afe32727a1f2/fnbeh-04-00014-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/c3848f3e3e8e/fnbeh-04-00014-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/aa6339ae5141/fnbeh-04-00014-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/8889b589e564/fnbeh-04-00014-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/127bde4a4bf8/fnbeh-04-00014-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/afe32727a1f2/fnbeh-04-00014-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/c3848f3e3e8e/fnbeh-04-00014-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/aa6339ae5141/fnbeh-04-00014-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/8889b589e564/fnbeh-04-00014-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/127bde4a4bf8/fnbeh-04-00014-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92ea/2854526/afe32727a1f2/fnbeh-04-00014-g005.jpg

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