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      Correction: Reelin controls the positioning of brainstem serotonergic raphe neurons

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          Abstract

          Fig 7 presents the 5-HT positive projections of the hindbrain serotonergic raphe neurons to the hippocampus in both wild type and reeler at postnatal day 20 (P20). The authors later discovered that the time point of used tissue was not from P20 but younger mice (P5). Please find the correct Fig 7 here, generated from brain tissue of WT and reeler mice of the correct age (P20). 10.1371/journal.pone.0211849.g001 Fig 7 Altered serotonergic innervation of the reeler hippocampus at P20. (A) Expression of Cxcr4-eGFP in Cajal-Retzius (CR) cells of the dentate gyrus. (B-D) Serotonergic fibers are distributed throughout hippocampal layers, and 5-HT positive fibers and Cajal-Retzius cells overlap. (E) Scattered distribution of Cajal-Retzius cells in reeler hippocampus. (F-H) Severe reduction of serotonergic fibers in Cxcr4-eGFP hippocampal reeler mice. CA1, cornu ammonis area 1; CA3, cornu ammonis area 3; DG, dentate gyrus. Scale bar for A-D: 100μm. In Fig 10, Fig 10H and Fig 10K were reversed accidentally. Fig 10H describes SERT positive fibers of serotonergic neurons into the hippocampus of reeler mice whereas Fig 10K describes SERT positive fibers of the serotonergic neurons into the hippocampus of WT mice. Please find the correct Fig 10 here, where the lower image (Fig 10K) has been be switched to the upper lane and vice versa. 10.1371/journal.pone.0211849.g002 Fig 10 Reduction of serotonin transporter protein (SERT) expression in brain regions of reeler mice. A. Western blot analysis showed reduction of SERT protein levels in reeler cortex, hippocampus, and Cerebellum as compared to wild type. (B-G) reduction of SERT expression in reeler cortex as well as in hippocampal slices as observed in (H-M) as compared to the same matched wild type littermates at P30. Hippo = hippocampus; Cereb = Cerebellum. Scale bar: 100 μm.

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          Reelin controls the positioning of brainstem serotonergic raphe neurons

          Serotonin (5-HT) acts as both a morphogenetic factor during early embryonic development and a neuromodulator of circuit plasticity in the mature brain. Dysregulation of serotonin signaling during critical periods is involved in developmental neurological disorders, such as schizophrenia and autism. In this study we focused on the consequences of defect reelin signaling for the development of the brainstem serotonergic raphe system. We observed that reelin signaling components are expressed by serotonergic neurons during the critical period of their lateral migration. Further, we found that reelin signaling is important for the normal migration of rostral, but not caudal hindbrain raphe nuclei and that reelin deficiency results in the malformation of the paramedian raphe nucleus and the lateral wings of the dorsal raphe nuclei. Additionally, we showed that serotonergic neurons projections to laminated brain structures were severely altered. With this study, we propose that the perturbation of canonical reelin signaling interferes with the orientation of tangentially, but not radially, migrating brainstem 5-HT neurons. Our results open the window for further studies on the interaction of reelin and serotonin and the pathogenesis of neurodevelopmental disorders.
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            Author and article information

            Journal
            PLoS One
            PLoS ONE
            plos
            plosone
            PLoS ONE
            Public Library of Science (San Francisco, CA USA )
            1932-6203
            31 January 2019
            2019
            31 January 2019
            : 14
            : 1
            : e0211849
            Article
            PONE-D-19-02321
            10.1371/journal.pone.0211849
            6355025
            30703171
            897911cb-6370-4443-9afc-b089703af7aa
            © 2019 Shehabeldin et al

            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 author and source are credited.

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