Profiles of Periglomerular Cells in the Olfactory Bulb of Prokineticin Type 2 Receptor-deficient Mice.
Profiles of Periglomerular Cells in the Olfactory Bulb of Prokineticin Type 2 Receptor-deficient Mice.
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DOI：
10.1267/ahc.17001
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发表时间：
2017-04-27
影响因子：
2.4
通讯作者：
Nagano M
中科院分区：
文献类型：
--
作者：
Kubo A;Sujino M;Masumoto KH;Fujioka A;Terashima T;Shigeyoshi Y;Nagano M
前动力蛋白受体2（pkr 2）和前动力蛋白2（pk 2）基因缺陷小鼠的主嗅球（MOB）发育不全。这种发育不良归因于由嗅觉感觉神经元（OSN）的传入投射损失引起的肾小球破坏，以及颗粒细胞（一种类型的中间神经元）的迁移受损。在本研究中，我们研究是否迁移的第二种类型的中间神经元，肾小球周围细胞（PGC），是依赖于pkr 2的表达，通过观察PGC的不同亚群的本地化：calretinin（CR），calbindin（CB）和酪氨酸羟化酶（TH）表达的神经元。在Pkr 2 −/−小鼠中，MOB的分层结构的构造部分保留，除了内部网状层（IPL）和肾小球层（GL）。在MOB的最外层，在发育不良的嗅球中观察到丰富的CR和CB免疫阳性神经元。此外，虽然明显减少，但在Pkr 2 −/−的最外层细胞密集区也观察到TH免疫阳性神经元。研究结果表明，PGC迁移到MOB，以及从MOB的核心到表面区域的迁移，不是由PK 2-PKR 2系统驱动的。
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.