Profiles of Periglomerular Cells in the Olfactory Bulb of Prokineticin Type 2 Receptor-deficient Mice

DOI Web Site 参考文献24件 オープンアクセス
  • Kubo Atsuko
    Department of Anatomy and Neurobiology, Kindai University Faculty of Medicine
  • Sujino Mitsugu
    Department of Anatomy and Neurobiology, Kindai University Faculty of Medicine
  • Masumoto Koh-hei
    Department of Anatomy and Neurobiology, Kindai University Faculty of Medicine
  • Fujioka Atsuko
    Department of Anatomy and Neurobiology, Kindai University Faculty of Medicine
  • Terashima Toshio
    Division of Anatomy and Developmental Neurobiology, Department of Cell Biology and Physiology, Kobe University Graduate School of Medicine
  • Shigeyoshi Yasufumi
    Department of Anatomy and Neurobiology, Kindai University Faculty of Medicine
  • Nagano Mamoru
    Department of Anatomy and Neurobiology, Kindai University Faculty of Medicine

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<p>Both prokineticin receptor 2 (pkr2) and prokineticin 2 (pk2) gene-deficient mice have hypoplasia of the main olfactory bulb (MOB). This hypoplasia has been attributed to disruption of the glomerulus that is caused by loss of afferent projection from olfactory sensory neurons (OSN), and to the impaired migration of granule cells, a type of interneuron. In the present study, we examined whether migration of the second type of interneuron, periglomerular cells (PGC), is dependent on the pkr2 expression by observing the localization of distinct subpopulations of PGC: calretinin (CR)-, calbindin (CB)- and tyrosine hydroxylase (TH)-expressing neurons. In the Pkr2−/− mice, the construction of the layered structure of the MOB was partially preserved, with the exception of the internal plexiform layer (IPL) and the glomerular layer (GL). In the outermost layer of the MOB, abundant CR- and CB-immunopositive neurons were observed in the hypoplastic olfactory bulb. In addition, although markedly decreased, TH-immunopositive neurons were also observed in the outermost cell-dense region in the Pkr2−/−. The findings suggest that the migration of PGC to the MOB, as well as the migration from the core to the surface region of the MOB, is not driven by the PK2-PKR2 system.</p>

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