Inamitsu M, Nakashima T, Uemura T
Department of Otolaryngology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
J Laryngol Otol. 1990 Dec;104(12):959-64. doi: 10.1017/s0022215100114483.
Removal of the olfactory bulb was performed on rats in an attempt to elucidate the processes of olfactory dysfunction following head injury. Degeneration and regeneration of the olfactory mucosa were examined, histopathologically and immunohistochemically. We used antisera to olfactory marker protein (OMP) and neuron specific enolase (NSE) as a marker of the mature olfactory receptor neurons. Following rapid degeneration after bulbectomy, the olfactory receptor neurons regenerated. OMP and NSE containing cells re-appeared 49 days later. However, the cell population of the neuroepithelium did not revert to the numbers observed in the non-operated neuroepithelium, even three months later. The lack of a connection between regenerated axons and the olfactory bulb may result in immature neuronal replacement and reduce the number of olfactory receptor neurons.
为了阐明头部受伤后嗅觉功能障碍的过程,对大鼠进行了嗅球切除。通过组织病理学和免疫组织化学方法检查了嗅黏膜的变性和再生情况。我们使用针对嗅觉标记蛋白(OMP)和神经元特异性烯醇化酶(NSE)的抗血清作为成熟嗅觉受体神经元的标记物。嗅球切除术后,嗅觉受体神经元迅速变性,随后再生。含OMP和NSE的细胞在49天后重新出现。然而,即使在三个月后,神经上皮细胞的数量也没有恢复到未手术神经上皮中观察到的数量。再生轴突与嗅球之间缺乏连接可能导致神经元替代不成熟,并减少嗅觉受体神经元的数量。