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      Structure, function, and pathology of Neurexin-3

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          Abstract

          Neurexin-3 is primarily localized in the presynaptic membrane and forms complexes with various ligands located in the postsynaptic membrane. Neurexin-3 has important roles in synapse development and synapse functions. Neurexin-3 mediates excitatory presynaptic differentiation by interacting with leucine-rich-repeat transmembrane neuronal proteins. Meanwhile, neurexin-3 modulates the expression of presynaptic α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors and γ-aminobutyric acid A receptors by interacting with neuroligins at excitatory and inhibitory synapses. Numerous studies have documented the potential contribution of neurexin-3 to neurodegenerative and neuropsychiatric disorders, such as Alzheimer's disease, addiction behaviors, and other diseases, which raises hopes that understanding the mechanisms of neurexin-3 may hold the key to developing new strategies for related illnesses. This review comprehensively covers the literature to provide current knowledge of the structure, function, and clinical role of neurexin-3.

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          Most cited references141

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          Genome-wide atlas of gene expression in the adult mouse brain.

          Molecular approaches to understanding the functional circuitry of the nervous system promise new insights into the relationship between genes, brain and behaviour. The cellular diversity of the brain necessitates a cellular resolution approach towards understanding the functional genomics of the nervous system. We describe here an anatomically comprehensive digital atlas containing the expression patterns of approximately 20,000 genes in the adult mouse brain. Data were generated using automated high-throughput procedures for in situ hybridization and data acquisition, and are publicly accessible online. Newly developed image-based informatics tools allow global genome-scale structural analysis and cross-correlation, as well as identification of regionally enriched genes. Unbiased fine-resolution analysis has identified highly specific cellular markers as well as extensive evidence of cellular heterogeneity not evident in classical neuroanatomical atlases. This highly standardized atlas provides an open, primary data resource for a wide variety of further studies concerning brain organization and function.
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            Mapping autism risk loci using genetic linkage and chromosomal rearrangements.

            Autism spectrum disorders (ASDs) are common, heritable neurodevelopmental conditions. The genetic architecture of ASDs is complex, requiring large samples to overcome heterogeneity. Here we broaden coverage and sample size relative to other studies of ASDs by using Affymetrix 10K SNP arrays and 1,181 [corrected] families with at least two affected individuals, performing the largest linkage scan to date while also analyzing copy number variation in these families. Linkage and copy number variation analyses implicate chromosome 11p12-p13 and neurexins, respectively, among other candidate loci. Neurexins team with previously implicated neuroligins for glutamatergic synaptogenesis, highlighting glutamate-related genes as promising candidates for contributing to ASDs.
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              Is there a common molecular pathway for addiction?

              Drugs of abuse have very different acute mechanisms of action but converge on the brain's reward pathways by producing a series of common functional effects after both acute and chronic administration. Some similar actions occur for natural rewards as well. Researchers are making progress in understanding the molecular and cellular basis of these common effects. A major goal for future research is to determine whether such common underpinnings of addiction can be exploited for the development of more effective treatments for a wide range of addictive disorders.
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                Author and article information

                Contributors
                Journal
                Genes Dis
                Genes Dis
                Genes & Diseases
                Chongqing Medical University
                2352-4820
                2352-3042
                30 April 2022
                September 2023
                30 April 2022
                : 10
                : 5
                : 1908-1919
                Affiliations
                [a ]Chongqing Key Laboratory of Neurobiology, Chongqing Medical University, Chongqing 400016, China
                [b ]Department of Neurology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing 400010, China
                [c ]Department of Anatomy, Chongqing Medical University, Chongqing 400016, China
                Author notes
                []Corresponding author. No.1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China. guiqionghe@ 123456cqmu.edu.cn
                [∗∗ ]Corresponding author. No.1 Yixueyuan Road, Yuzhong District, Chongqing 400016, China. liuyuanjie@ 123456cqmu.edu.cn
                Article
                S2352-3042(22)00106-4
                10.1016/j.gendis.2022.04.008
                10363586
                37492720
                2d43a125-0637-44dc-b2e1-b479cf9294cc
                © 2022 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 26 August 2021
                : 6 April 2022
                : 8 April 2022
                Categories
                Review Article

                excitatory synapses,inhibitory synapses,neural cell adhesion molecules,neurexin-3,neurodegenerative diseases,neuropsychiatric diseases

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