Suppr超能文献

自闭症的细胞与神经回路基础:从大脑中自闭症基因的时空操纵中获得的经验教训。

Cellular and Circuitry Bases of Autism: Lessons Learned from the Temporospatial Manipulation of Autism Genes in the Brain.

作者信息

Hulbert Samuel W, Jiang Yong-Hui

机构信息

Department of Neurobiology, School of Medicine, Duke University, Durham, NC, 27710, USA.

Department of Pediatrics, School of Medicine, Duke University, Durham, NC, 27710, USA.

出版信息

Neurosci Bull. 2017 Apr;33(2):205-218. doi: 10.1007/s12264-017-0112-7. Epub 2017 Mar 7.

Abstract

Transgenic mice carrying mutations that cause Autism Spectrum Disorders (ASDs) continue to be valuable for determining the molecular underpinnings of the disorders. Recently, researchers have taken advantage of such models combined with Cre-loxP and similar systems to manipulate gene expression over space and time. Thus, a clearer picture is starting to emerge of the cell types, circuits, brain regions, and developmental time periods underlying ASDs. ASD-causing mutations have been restricted to or rescued specifically in excitatory or inhibitory neurons, different neurotransmitter systems, and cells specific to the forebrain or cerebellum. In addition, mutations have been induced or corrected in adult mice, providing some evidence for the plasticity and reversibility of core ASD symptoms. The limited availability of Cre lines that are highly specific to certain cell types or time periods provides a challenge to determining the cellular and circuitry bases of autism, but other technological advances may eventually overcome this obstacle.

摘要

携带导致自闭症谱系障碍(ASD)突变的转基因小鼠对于确定这些疾病的分子基础仍然具有重要价值。最近,研究人员利用此类模型结合Cre-loxP及类似系统,在空间和时间上操纵基因表达。因此,关于ASD背后的细胞类型、神经回路、脑区和发育时间段的更清晰图景开始浮现。导致ASD的突变已被限制在兴奋性或抑制性神经元、不同神经递质系统以及前脑或小脑特有的细胞中,或在这些细胞中得到特异性挽救。此外,已在成年小鼠中诱导或纠正突变,为ASD核心症状的可塑性和可逆性提供了一些证据。高度特异性针对某些细胞类型或时间段的Cre品系数量有限,这给确定自闭症的细胞和神经回路基础带来了挑战,但其他技术进步最终可能克服这一障碍。

相似文献

1
Cellular and Circuitry Bases of Autism: Lessons Learned from the Temporospatial Manipulation of Autism Genes in the Brain.
Neurosci Bull. 2017 Apr;33(2):205-218. doi: 10.1007/s12264-017-0112-7. Epub 2017 Mar 7.
2
Modeling non-syndromic autism and the impact of TRPC6 disruption in human neurons.
Mol Psychiatry. 2015 Nov;20(11):1350-65. doi: 10.1038/mp.2014.141. Epub 2014 Nov 11.
3
Autism-relevant behaviors are minimally impacted by conditional deletion of Pten in oxytocinergic neurons.
Autism Res. 2016 Dec;9(12):1248-1262. doi: 10.1002/aur.1641. Epub 2016 May 25.
5
Mutation of the CH1 Domain in the Histone Acetyltransferase CREBBP Results in Autism-Relevant Behaviors in Mice.
PLoS One. 2016 Jan 5;11(1):e0146366. doi: 10.1371/journal.pone.0146366. eCollection 2016.
6
Neuroligin-3-deficient mice: model of a monogenic heritable form of autism with an olfactory deficit.
Genes Brain Behav. 2009 Jun;8(4):416-25. doi: 10.1111/j.1601-183X.2009.00487.x. Epub 2009 Feb 11.
7
Autism-like behaviours and germline transmission in transgenic monkeys overexpressing MeCP2.
Nature. 2016 Feb 4;530(7588):98-102. doi: 10.1038/nature16533. Epub 2016 Jan 25.
8
The role of neurotrophic factors in autism.
Mol Psychiatry. 2011 May;16(5):478-90. doi: 10.1038/mp.2010.103. Epub 2010 Oct 12.
9
Inducible gene inactivation in neurons of the adult mouse forebrain.
BMC Neurosci. 2007 Aug 2;8:63. doi: 10.1186/1471-2202-8-63.
10
Agmatine rescues autistic behaviors in the valproic acid-induced animal model of autism.
Neuropharmacology. 2017 Feb;113(Pt A):71-81. doi: 10.1016/j.neuropharm.2016.09.014. Epub 2016 Sep 14.

引用本文的文献

4
Modeling Autism Spectrum Disorders with Induced Pluripotent Stem Cell-Derived Brain Organoids.
Biomolecules. 2023 Jan 30;13(2):260. doi: 10.3390/biom13020260.
6
Oxytocin Receptor in Cerebellar Purkinje Cells Does Not Engage in Autism-Related Behaviors.
Cerebellum. 2023 Oct;22(5):888-904. doi: 10.1007/s12311-022-01466-5. Epub 2022 Aug 30.
7
New Concerns for Neurocognitive Function during Deep Space Exposures to Chronic, Low Dose-Rate, Neutron Radiation.
eNeuro. 2019 Aug 22;6(4). doi: 10.1523/ENEURO.0094-19.2019. Print 2019 Jul/Aug.
8
Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons.
Mol Autism. 2018 Dec 19;9:65. doi: 10.1186/s13229-018-0244-2. eCollection 2018.

本文引用的文献

2
Lessons learned from studying syndromic autism spectrum disorders.
Nat Neurosci. 2016 Oct 26;19(11):1408-1417. doi: 10.1038/nn.4420.
7
SHANK3 controls maturation of social reward circuits in the VTA.
Nat Neurosci. 2016 Jul;19(7):926-934. doi: 10.1038/nn.4319. Epub 2016 Jun 6.
8
Autism-relevant behaviors are minimally impacted by conditional deletion of Pten in oxytocinergic neurons.
Autism Res. 2016 Dec;9(12):1248-1262. doi: 10.1002/aur.1641. Epub 2016 May 25.
10
Loss of MeCP2 in cholinergic neurons causes part of RTT-like phenotypes via α7 receptor in hippocampus.
Cell Res. 2016 Jun;26(6):728-42. doi: 10.1038/cr.2016.48. Epub 2016 Apr 22.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验