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The PROK2 (prokineticin 2) and PROKR2 (prokineticin receptor 2) signaling pathway has been identified to cause human Kallmann syndrome, a developmental disease that associates hypogonadism with anosmia (OB developmental defects). However, the identities and properties of PROK2\n                    <jats:sup>+<\/jats:sup>\n                    and PROKR2\n                    <jats:sup>+<\/jats:sup>\n                    cells in the SVZ\u2010RMS\u2010OB remain largely unknown. Here we examine the expression patterns of\n                    <jats:italic>Prok2<\/jats:italic>\n                    and\n                    <jats:italic>Prokr2<\/jats:italic>\n                    in the SVZ\u2010RMS\u2010OB using\n                    <jats:italic>Prok2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>EGFP<\/jats:italic>\n                    <\/jats:sup>\n                    transgenic and\n                    <jats:italic>Prokr2<\/jats:italic>\n                    <jats:sup>\n                      <jats:italic>LacZ\/+<\/jats:italic>\n                    <\/jats:sup>\n                    knockin mice. Our results show that\n                    <jats:italic>Prokr2<\/jats:italic>\n                    is expressed in postmitotic immature interneurons in the SVZ\u2010RMS\u2010OB.\n                    <jats:italic>Prok2<\/jats:italic>\n                    is not expressed in the SVZ, but a few PROK2\n                    <jats:sup>\n                      <jats:italic>+<\/jats:italic>\n                    <\/jats:sup>\n                    cells are found in the medial part of the RMS; they are not neural progenitors or migrating neuroblasts. In the OB,\n                    <jats:italic>Prok2<\/jats:italic>\n                    is expressed in a subset of granule cells and tufted cells, but no coexpression of\n                    <jats:italic>Prok2<\/jats:italic>\n                    and\n                    <jats:italic>Prokr2<\/jats:italic>\n                    in the OB cells is observed. In\n                    <jats:italic>Prok2<\/jats:italic>\n                    and\n                    <jats:italic>Prokr2<\/jats:italic>\n                    mutant mice, severe tangential and radial migration defects of neuroblasts in the SVZ\u2010RMS\u2010OB result in loss of ~75% of GABAergic interneurons in the OB. These analyses demonstrate that PROK2\/PROKR2 signaling is crucial for the tangential and radial migration of OB interneurons.\n                  <\/jats:p>","DOI":"10.1002\/cne.24719","type":"journal-article","created":{"date-parts":[[2019,5,27]],"date-time":"2019-05-27T10:04:24Z","timestamp":1558951464000},"page":"2931-2947","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["The PROK2\/PROKR2 signaling pathway is required for the migration of most olfactory bulb interneurons"],"prefix":"10.1002","volume":"527","author":[{"given":"Yan","family":"Wen","sequence":"first","affiliation":[{"name":"State Key Laboratory of Medical Neurobiology, Institutes of Brain Science, MOE Frontier Center for Brain Science, Department of Neurology, Zhongshan Hospital Fudan University  Shanghai PR 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