@article{9b13eec2e00c40098d305bd31708079f,
title = "A morphometric study of the pallid mutant mouse inner ear",
abstract = "Mice homozygous for the mutant gene pallid (pa/pa) often lack otoconia in some or all of their maculae and are used to study the influences of gravity receptor hypostimulation on vestibular-related behaviors. Since the value of this animal model is based on the assumption that the vestibular sensorineural elements are normal, a morphometric analysis was done on the inner ear of these otoconia-deficient mice to see whether sensorineural structures are also affected by the pallid gene. In pallid mice lacking all otoconia, the sensory epithelia of the utricle, saccule, and semicircular canal cristae were the same size as in their heterozygous (pa/+) controls. Although the superior and inferior divisions of the vestibular ganglion of the pallid mice were smaller than normal, the first-order neurons within these divisions were normal in size, number, and density. However, the superior divisions in both groups had larger neurons than did the inferior divisions. Within the pallid cochlea, first-order auditory neurons within the spiral ganglion were smaller than normal, but the scala media was larger. Since the significant vestibular influences of the pallid gene are limited primarily to the otoconia, behavioral abnormalities reported for these otoconia-deficient mice are apparently due only to gravity receptor hypostimulation.",
keywords = "Cochlea, Morphometry, Otoconia, Pallid mouse, Vestibule",
author = "Trune, {Dennis R.} and Lim, {David J.}",
note = "Funding Information: Lyon 1,2 first described the absence of otoconia in the inner ears of mice homozygous for the recessive, mutant gene pallid (pa). Although all homozygotes (pa/pa) have the pale coat color and unpigmented eye, the penetrance of the otoconial effect is incomplete and can range, within the same animal, from no otoconia in any of the gravity receptors to normal otoconia in some or all receptors. Also, the pa gene is considered pleiotropic, since otoconial loss is never observed without the lack of pigmentation, and it is apparently responsible for both the otoconia and pigment defects. Mutants in which otoconia deficiency is a predominant characteristic have been observed among a variety of species, most of which also have an associated pigment defect. These include the mutant mice mocha, 3 tilted-head, 4 and lethal-milk, 5 as well as the ocular albino rabbit, gray-loco chukar partridge, pastel mink, 6 octopus, cuttlefish, and squid. 7 Recently, otoconia deficiency was also observed in hu- Laboratories, Department of Otolaryngology,T he Ohio State University College of Medicine, Columbus, Ohio. Accepted for publication April 7, 1983. Supported by National Aeronautics and Space Administrationg rant NSG-2220 (to D.J.L.) and National Institutes of Health grant NINCDS-NRSA 5 F32 NSO6211 (to D.R.T.). Address correspondence and reprint requests to Dr. Trune: Otological Research Laboratories, 4331 UniversityH ospitals Clinic, 456 Clinic Drive, Columbus, OH 43210. Copyright: Copyright 2014 Elsevier B.V., All rights reserved.",
year = "1983",
doi = "10.1016/S0196-0709(83)80070-2",
language = "English (US)",
volume = "4",
pages = "261--272",
journal = "American Journal of Otolaryngology--Head and Neck Medicine and Surgery",
issn = "0196-0709",
publisher = "W.B. Saunders Ltd",
number = "4",
}