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.

中文翻译：

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Prokineticin 2型受体缺陷型小鼠嗅球中的小球周围细胞的概况。

prokineticin受体2（pkr2）和prokineticin 2（pk2）基因缺陷小鼠均具有主要嗅球（MOB）发育不全。这种发育不全的原因是由于嗅觉感觉神经元（OSN）的传入投射的丧失导致肾小球的破坏，以及粒间细胞（一种中间神经元）的迁移受损。在本研究中，我们通过观察PGC的不同亚群的定位：钙调蛋白（CR）-，钙结合蛋白（CB）-和PKC2，检查了第二种类型的中间神经元，肾小球周围细胞（PGC）的迁移是否依赖于pkr2表达。表达酪氨酸羟化酶（TH）的神经元。在Pkr2-/-小鼠中，除内部丛状层（IPL）和肾小球层（GL）外，部分保留了MOB分层结构的结构。在MOB的最外层，在发育不良的嗅球中观察到大量的CR和CB免疫阳性神经元。另外，尽管Pkr2-/-最外层的细胞密集区也观察到TH-免疫阳性神经元，尽管明显减少。研究结果表明，PGC到MOB的迁移以及从MOB的核心到表面区域的迁移不受PK2-PKR2系统的驱动。