Abstract |
This study documents morphologic alterations in the spiral ganglion and Scarpa's ganglion from gamma-aminobutyric acid A ( GABA(A)) receptor beta(3) subunit null mutant mice. The ganglion cells of the mutant mice were hypoplastic in hematoylin& eosin-stained sections. Hypoplasia was observed at every location of the spiral ganglion and Scarpa's ganglion except the apical cochlear turn. Calretinin immunostaining demonstrated a selective hypoplasia of calretinin-negative cells at every location of spiral and Scarpa's ganglion cells, while the soma area of calretinin-positive cells was not affected by the gene deletion. Meanwhile, in the spiral ganglion of both wild type and knockout mice, there were apical to basal gradients in the soma size and the proportion of calretinin-positive cells. The absence of statistically significant hypoplasia in hematoylin& eosin sections through the apical turn of the cochlea can be explained by the relatively higher proportion of calretinin-positive ganglion cells, which were unaffected by the gene deletion. These findings suggest that GABA(A) receptor isoforms containing the beta(3) subunit may play an important role in the development and differentiation of non-calyceal terminals of Scarpa's ganglion cells and type II and smaller type I spiral ganglion cells.
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Authors | Ja-Won Koo, Gregg E Homanics, Carey D Balaban |
Journal | Hearing research
(Hear Res)
Vol. 167
Issue 1-2
Pg. 71-80
(May 2002)
ISSN: 0378-5955 [Print] Netherlands |
PMID | 12117532
(Publication Type: Journal Article)
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Chemical References |
- Calb2 protein, mouse
- Calbindin 2
- Protein Subunits
- Receptors, GABA-A
- S100 Calcium Binding Protein G
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Topics |
- Animals
- Calbindin 2
- Cell Differentiation
- Cell Size
- Immunohistochemistry
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
- Protein Subunits
- Receptors, GABA-A
(chemistry, deficiency, genetics, physiology)
- S100 Calcium Binding Protein G
(metabolism)
- Spiral Ganglion
(abnormalities, metabolism, pathology)
- Vestibular Nerve
(abnormalities, metabolism, pathology)
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