Effects of early hypophysectomy on the development of the otic capsule and tympanic bulla of rats

Marovitz, William F.; Berryhill, Bruce H.; Gregory, Kenneth M.

doi:10.1288/00005537-196710000-00004

Cited by 5 publications

(2 citation statements)

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“…Guggenheim (1943) reported that some rats in a strain born deaf and known to have unusual amounts of tympanal mesenchyme regained their hearing and showed marked diminution in the amount of embryonal tissue when injected with anterior pituitary extract. Long-Evans rat (Marovitz et al, 1967;1968a) and the dwarf Snell mouse (Marovitz et al, 1968b) have been used as animal models for study of abnormal development in the middle ear. Removal of rat pituitary directly disrupts temporal bone and ossicular chain growth and maturation by the deletion of pituitary growth hormone and indirectly by the elimination of thyroxin (Marovitz et al, 1967).…”

Section: Discussionmentioning

confidence: 99%

“…Long-Evans rat (Marovitz et al, 1967;1968a) and the dwarf Snell mouse (Marovitz et al, 1968b) have been used as animal models for study of abnormal development in the middle ear. Removal of rat pituitary directly disrupts temporal bone and ossicular chain growth and maturation by the deletion of pituitary growth hormone and indirectly by the elimination of thyroxin (Marovitz et al, 1967). Mesenchyme in dwarf Snell mice remains in an uncavitated state (Marovitz et al, 1968b).…”

Section: Discussionmentioning

confidence: 99%

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Apoptosis in cavitation of middle ear space

Roberts¹,

Miller²

1998

Anat. Rec.

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Mesenchyme cells surround early ossicles in the developing middle ear, then are replaced by space that is created by what has been described as an expansion of the pharyngeal pouch. Cell death has not been considered important in cavitation of chick middle ear (Jaskoll and Maderson [1978] Anat. Rec., 190:177-200), but an uncharacterized form of cell death has been reported to play a major role in cavitation of mouse middle ear (Jaskoll [1977] PhD thesis, CUNY). We investigated whether this uncharacterized cell death is the non-random form known as apoptosis. We examined the middle ear cavitation process using an in situ immunomarker for apoptosis. CBy RF mice during prenatal days 15-20 and postnatal days 1-3 and chick embryos representing HH stages 33-38 were investigated. Apoptotic cells were marked in mouse postnatal day 1. No indication of apoptosis was present in other prenatal and postnatal days of development included in this study, although morphology showed that cavitation proceeds over several perinatal days in the mouse. Apoptosis was not marked in the chick middle ear. Previously observed cell death in murine middle ear is the non-random form of cell death known as apoptosis. Cell death has not been reported in avian middle ear, and lack of apoptotic marker supports those observations. The limited occurrence of apoptosis in mice and apparent absence of apoptosis in chicks suggest that several mechanisms contribute to cavitation of vertebrate middle ear space.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Apoptosis in cavitation of middle ear space

Roberts¹,

Miller²

1998

Anat. Rec.

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Thyroid Hormone Receptors Control Developmental Maturation of the Middle Ear and the Size of the Ossicular Bones

Cordas

Hernández³

et al. 2012

Endocrinology

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Thyroid hormone is critical for auditory development and has well-known actions in the inner ear. However, less is known of thyroid hormone functions in the middle ear, which contains the ossicles (malleus, incus, stapes) that relay mechanical sound vibrations from the outer ear to the inner ear. During the later stages of middle ear development, prior to the onset of hearing, middle ear cavitation occurs, involving clearance of mesenchyme from the middle ear cavity while the immature cartilaginous ossicles attain appropriate size and ossify. Using in situ hybridization, we detected expression of Thra and Thrb genes encoding thyroid hormone receptors α1 and β (TRα1 and TRβ, respectively) in the immature ossicles, surrounding mesenchyme and tympanic membrane in the mouse. Thra(+/PV) mice that express a dominant-negative TRα1 protein exhibited deafness with elevated auditory thresholds and a range of middle ear abnormalities including chronic persistence of mesenchyme in the middle ear into adulthood, markedly enlarged ossicles, and delayed ossification of the ossicles. Congenitally hypothyroid Tshr(-/-) mice and TR-deficient Thra1(-/-);Thrb(-/-) mice displayed similar abnormalities. These findings demonstrate that middle ear maturation is TR dependent and suggest that the middle ear is a sensitive target for thyroid hormone in development.

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