Literature DB >> 9700571

Ultrastructure of the olfactory organ in the clawed frog, Xenopus laevis, during larval development and metamorphosis.

A Hansen1, J O Reiss, C L Gentry, G D Burd.   

Abstract

Development of the olfactory epithelia of the African clawed frog, Xenopus laevis, was studied by scanning and transmission electron microscopy. Stages examined ranged from hatching through the end of metamorphosis. The larval olfactory organ consists of two chambers, the principal cavity and the vomeronasal organ (VNO). A third sensory chamber, the middle cavity, arises during metamorphosis. In larvae, the principal cavity is exposed to water-borne odorants, but after metamorphosis it is exposed to airborne odorants. The middle cavity and the VNO are always exposed to waterborne odorants. Electron microscopy reveals that in larvae, principal cavity receptor cells are of two types, ciliated and microvillar. Principal cavity supporting cells are also of two types, ciliated and secretory (with small, electron-lucent granules). After metamorphosis, the principal cavity contains only ciliated receptor cells and secretory supporting cells, and the cilia on the receptor cells are longer than in larvae. Supporting cell secretory granules are now large and electron-dense. In contrast, the middle cavity epithelium contains the same cell types seen in the larval principal cavity. The VNO has microvillar receptor cells and ciliated supporting cells throughout life. The cellular process by which the principal cavity epithelium changes during metamorphosis is not entirely clear. Morphological evidence from this study suggests that both microvillar and ciliated receptor cells die, to be replaced by newly generated cells. In addition, ciliated supporting cells also appear to die, whereas there is evidence that secretory supporting cells transdifferentiate into the adult type. In summary, significant developmental additions and neural plasticity are involved in remodeling the olfactory epithelium in Xenopus at metamorphosis.

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Year:  1998        PMID: 9700571     DOI: 10.1002/(sici)1096-9861(19980824)398:2<273::aid-cne8>3.0.co;2-y

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


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