The Vestibular System (Springer Handbook of Auditory by Stephen M. Highstein, Richard R. Fay, Arthur N. Popper

By Stephen M. Highstein, Richard R. Fay, Arthur N. Popper

The Springer guide of Auditory study offers a sequence of man-made reports of basic subject matters facing auditory structures. each one quantity is self sustaining and authoritative; taken as a collection, this sequence stands out as the definitive source within the box. This quantity features a coherent choice of artificial studies at the vestibular method: the part of our auditory and worried platforms that's chargeable for our feel of stability. This quantity may be of curiosity to neuroscientists and otolaryngologists interested by learning the vestibular and auditory senses.

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It was proposed that the lack of proliferation in the surrounding mesenchyme fails to drive 2. Molecular Genetics of Vestibular Organ Development 37 the opposing otic epithelia of the outpocket to come together to form the fusion plate (Salminen et al. 2000). Nor-1 is a member of the nuclear receptor family of transcription factors. Members of this subclass of nuclear receptors are thought to function as constitutively active transcription factors (Maruyama et al. 1998). A ligand for Nor-1, if one exists, has not been identified.

During later stages of development, the expression domains of both of these genes are restricted to nonsensory cells within each sensory patch (Lewis et al. 1998; Morrison et al. 1999; Shailam et al. 1999). Recent data suggest that the function of the Notch signaling pathway is not restricted to hair cell/supporting cell determination in the inner ear but is also required for the patterning of the ampulla and canal. Two mouse mutants, Headturner and Slalom, with missense mutations in the Notch ligand, Jagged1, have recently been characterized.

2000). Presumably, Ngn1 is acting upstream of NeuroD and functions in a pathway similar to NeuroD in the 2. Molecular Genetics of Vestibular Organ Development 33 development of sensory neurons (Ma et al. 1998). Gene expression analyses of Shh knockout mice as well as a transgenic line that ectopically expresses Shh in the otic vesicle (ShhP1) suggest that Shh may act upstream of Ngn1 (Riccomagno et al. 2002). In Shh knockout mice, Ngn1 and NeuroD are down-regulated and the cochleovestibular ganglia are greatly reduced in size.

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