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      Transcriptomics reveals amygdala neuron regulation by fasting and ghrelin thereby promoting feeding

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          Abstract

          The central amygdala (CeA) consists of numerous genetically defined inhibitory neurons that control defensive and appetitive behaviors including feeding. Transcriptomic signatures of cell types and their links to function remain poorly understood. Using single-nucleus RNA sequencing, we describe nine CeA cell clusters, of which four are mostly associated with appetitive and two with aversive behaviors. To analyze the activation mechanism of appetitive CeA neurons, we characterized serotonin receptor 2a (Htr2a)–expressing neurons (CeA Htr2a) that comprise three appetitive clusters and were previously shown to promote feeding. In vivo calcium imaging revealed that CeA Htr2a neurons are activated by fasting, the hormone ghrelin, and the presence of food. Moreover, these neurons are required for the orexigenic effects of ghrelin. Appetitive CeA neurons responsive to fasting and ghrelin project to the parabrachial nucleus (PBN) causing inhibition of target PBN neurons. These results illustrate how the transcriptomic diversification of CeA neurons relates to fasting and hormone-regulated feeding behavior.

          Abstract

          Central amygdala neuron diversity and the roles of appetitive amygdala neurons in hormone-regulated feeding behavior are unveiled.

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          A robust and high-throughput Cre reporting and characterization system for the whole mouse brain

          Linda Madisen, Theresa Zwingman, Susan M. Sunkin … (2009)
          The Cre/lox system is widely used in mice to achieve cell-type-specific gene expression. However, a strong and universal responding system to express genes under Cre control is still lacking. We have generated a set of Cre reporter mice with strong, ubiquitous expression of fluorescent proteins of different spectra. The robust native fluorescence of these reporters enables direct visualization of fine dendritic structures and axonal projections of the labeled neurons, which is useful in mapping neuronal circuitry, imaging and tracking specific cell populations in vivo. Using these reporters and a high-throughput in situ hybridization platform, we are systematically profiling Cre-directed gene expression throughout the mouse brain in a number of Cre-driver lines, including novel Cre lines targeting different cell types in the cortex. Our expression data are displayed in a public online database to help researchers assess the utility of various Cre-driver lines for cell-type-specific genetic manipulation.
          Article 0 comments Cited 1455 times – based on 0 reviews     Review now
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            DAVID: a web server for functional enrichment analysis and functional annotation of gene lists (2021 update).

            Brad T. Sherman, Ming Hao, Ju Qiu … (2022)
            DAVID is a popular bioinformatics resource system including a web server and web service for functional annotation and enrichment analyses of gene lists. It consists of a comprehensive knowledgebase and a set of functional analysis tools. Here, we report all updates made in 2021. The DAVID Gene system was rebuilt to gain coverage of more organisms, which increased the taxonomy coverage from 17 399 to 55 464. All existing annotation types have been updated, if available, based on the new DAVID Gene system. Compared with the last version, the number of gene-term records for most annotation types within the updated Knowledgebase have significantly increased. Moreover, we have incorporated new annotations in the Knowledgebase including small molecule-gene interactions from PubChem, drug-gene interactions from DrugBank, tissue expression information from the Human Protein Atlas, disease information from DisGeNET, and pathways from WikiPathways and PathBank. Eight of ten subgroups split from Uniprot Keyword annotation were assigned to specific types. Finally, we added a species parameter for uploading a list of gene symbols to minimize the ambiguity between species, which increases the efficiency of the list upload and eliminates confusion for users. These current updates have significantly expanded the Knowledgebase and enhanced the discovery power of DAVID.
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              Single-cell transcriptomic analysis of Alzheimer’s disease

              Hansruedi Mathys, Jose Davila-Velderrain, Zhuyu Peng … (2019)
              Alzheimer's disease is a pervasive neurodegenerative disorder, the molecular complexity of which remains poorly understood. Here, we analysed 80,660 single-nucleus transcriptomes from the prefrontal cortex of 48 individuals with varying degrees of Alzheimer's disease pathology. Across six major brain cell types, we identified transcriptionally distinct subpopulations, including those associated with pathology and characterized by regulators of myelination, inflammation, and neuron survival. The strongest disease-associated changes appeared early in pathological progression and were highly cell-type specific, whereas genes upregulated at late stages were common across cell types and primarily involved in the global stress response. Notably, we found that female cells were overrepresented in disease-associated subpopulations, and that transcriptional responses were substantially different between sexes in several cell types, including oligodendrocytes. Overall, myelination-related processes were recurrently perturbed in multiple cell types, suggesting that myelination has a key role in Alzheimer's disease pathophysiology. Our single-cell transcriptomic resource provides a blueprint for interrogating the molecular and cellular basis of Alzheimer's disease.
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                Author and article information

                Contributors
                Christian Peters:
                ORCID: https://orcid.org/0000-0001-5033-6571
                Role: ConceptualizationRole: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: Project administrationRole: ValidationRole: VisualizationRole: Writing - original draftRole: Writing - review & editing
                Songwei He:
                ORCID: https://orcid.org/0000-0002-9137-1696
                Role: ConceptualizationRole: Data curationRole: Formal analysisRole: InvestigationRole: MethodologyRole: ResourcesRole: SoftwareRole: ValidationRole: VisualizationRole: Writing - original draftRole: Writing - review & editing
                Federica Fermani:
                ORCID: https://orcid.org/0000-0002-4113-3091
                Role: ConceptualizationRole: Formal analysisRole: InvestigationRole: MethodologyRole: VisualizationRole: Writing - review & editing
                Hansol Lim: Role: Investigation
                Wenyu Ding: Role: InvestigationRole: Validation
                Christian Mayer:
                ORCID: https://orcid.org/0000-0003-3152-5574
                Role: ConceptualizationRole: SoftwareRole: Validation
                Rüdiger Klein:
                ORCID: https://orcid.org/0000-0002-3109-0163
                Role: ConceptualizationRole: Funding acquisitionRole: Project administrationRole: SupervisionRole: Writing - original draftRole: Writing - review & editing
                Journal
                Journal ID (nlm-ta): Sci Adv
                Journal ID (iso-abbrev): Sci Adv
                Journal ID (publisher-id): sciadv
                Journal ID (hwp): advances
                Title: Science Advances
                Publisher: American Association for the Advancement of Science
                ISSN (Electronic): 2375-2548
                Publication date Collection: May 2023
                Publication date (Electronic, pub): 24 May 2023
                Volume: 9
                Issue: 21
                Electronic Location Identifier: eadf6521
                Affiliations
                [ 1 ]Department of Molecules–Signaling–Development, Max-Planck Institute for Biological Intelligence, 82152 Martinsried, Germany.
                [ 2 ]Laboratory of Neurogenomics, Max-Planck Institute for Biological Intelligence, 82152 Martinsried, Germany.
                Author notes
                [* ]Corresponding author. Email: ruediger.klein@ 123456bi.mpg.de
                Author information
                https://orcid.org/0000-0001-5033-6571
                https://orcid.org/0000-0002-9137-1696
                https://orcid.org/0000-0002-4113-3091
                https://orcid.org/0000-0003-3152-5574
                https://orcid.org/0000-0002-3109-0163
                Article
                Publisher ID: adf6521
                DOI: 10.1126/sciadv.adf6521
                PMC ID: 10208581
                PubMed ID: 37224253
                SO-VID: 3442ba27-7d47-4d68-b3c3-250d55e2a009
                Copyright © Copyright © 2023 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY).
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution license, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 04 November 2022
                Date accepted : 19 April 2023
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/100010661, Horizon 2020 Framework Programme;
                Award ID: 885192
                Funded by: FundRef http://dx.doi.org/10.13039/100019180, HORIZON EUROPE European Research Council;
                Award ID: 885192
                Funded by: Max Planck Society;
                Categories
                Subject: Research Article
                Subject: Neuroscience
                Subject: SciAdv r-articles
                Subject: Neurophysiology
                Subject: Neuroscience
                Subject: Neurophysiology
                Custom metadata
                Copyeditor Mjoy Azul

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