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蜜蜂大脑中神经连接蛋白和神经连接素 I 的感觉调节。

Sensory regulation of neuroligins and neurexin I in the honeybee brain.

机构信息

Queensland Brain Institute, The University of Queensland, St Lucia, Queensland, Australia.

出版信息

PLoS One. 2010 Feb 9;5(2):e9133. doi: 10.1371/journal.pone.0009133.

DOI:10.1371/journal.pone.0009133
PMID:20161754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2817746/
Abstract

BACKGROUND

Neurexins and neuroligins, which have recently been associated with neurological disorders such as autism in humans, are highly conserved adhesive proteins found on synaptic membranes of neurons. These binding partners produce a trans-synaptic bridge that facilitates maturation and specification of synapses. It is believed that there exists an optimal spatio-temporal code of neurexin and neuroligin interactions that guide synapse formation in the postnatal developing brain. Therefore, we investigated whether neuroligins and neurexin are differentially regulated by sensory input using a behavioural model system with an advanced capacity for sensory processing, learning and memory, the honeybee.

METHODOLOGY/PRINCIPAL FINDINGS: Whole brain expression levels of neuroligin 1-5 (NLG1-5) and neurexin I (NrxI) were estimated by qRT-PCR analysis in three different behavioural paradigms: sensory deprivation, associative scent learning, and lateralised sensory input. Sensory deprived bees had a lower level of NLG1 expression, but a generally increased level of NLG2-5 and NrxI expression compared to hive bees. Bees that had undergone associative scent training had significantly increased levels of NrxI, NLG1 and NLG3 expression compared to untrained control bees. Bees that had lateralised sensory input after antennal amputation showed a specific increase in NLG1 expression compared to control bees, which only happened over time.

CONCLUSIONS/SIGNIFICANCE: Our results suggest that (1) there is a lack of synaptic pruning during sensory deprivation; (2) NLG1 expression increases with sensory stimulation; (3) concomitant changes in gene expression suggests NrxI interacts with all neuroligins; (4) there is evidence for synaptic compensation after lateralised injury.

摘要

背景

神经连接素和神经黏连蛋白最近与人的自闭症等神经紊乱有关,是在神经元突触膜上高度保守的黏附蛋白。这些结合伴侣产生一个跨突触桥,促进突触的成熟和特化。人们相信存在一个神经连接素和神经黏连蛋白相互作用的最优时空编码,指导出生后发育大脑中的突触形成。因此,我们使用具有先进感觉处理、学习和记忆能力的行为模型系统——蜜蜂,研究了神经黏连蛋白和神经连接素是否因感觉输入而受到差异调控。

方法/主要发现:通过 qRT-PCR 分析,在三种不同的行为范式中,即感觉剥夺、联想气味学习和单侧感觉输入,估计了神经黏连蛋白 1-5(NLG1-5)和神经连接素 I(NrxI)的全脑表达水平。与蜂巢蜜蜂相比,感觉剥夺蜜蜂的 NLG1 表达水平较低,但 NLG2-5 和 NrxI 的表达水平普遍升高。接受联想气味训练的蜜蜂与未接受训练的对照蜜蜂相比,NrxI、NLG1 和 NLG3 的表达水平显著增加。与对照蜜蜂相比,触角截肢后单侧感觉输入的蜜蜂 NLG1 表达特异性增加,这种增加仅随时间发生。

结论/意义:我们的结果表明:(1)在感觉剥夺期间不存在突触修剪;(2)NLG1 表达随感觉刺激增加;(3)伴随基因表达的变化表明 NrxI 与所有神经黏连蛋白相互作用;(4)存在单侧损伤后的突触补偿证据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d35/2817746/40e3b05ac333/pone.0009133.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d35/2817746/4f6abc81a08f/pone.0009133.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d35/2817746/995ceffd9e5c/pone.0009133.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d35/2817746/40e3b05ac333/pone.0009133.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d35/2817746/4f6abc81a08f/pone.0009133.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d35/2817746/995ceffd9e5c/pone.0009133.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d35/2817746/40e3b05ac333/pone.0009133.g003.jpg

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