Literature DB >> 12687710

Olivocochlear efferent innervation of the organ of corti in hypothyroid rats.

Raquel Cantos1, Dolores E López, Jaime A Merchán, Joaquín Rueda.   

Abstract

Congenital hypothyroidism induces developmental abnormalities in the auditory receptor, causing deafness due to a poor development of the outer hair cells (OHCs) and a lack of synaptogenesis between these cells and the olivocochlear axons. This efferent innervation is formed by two separate systems: the lateral system, which originates in the lateral superior olive (LSO) and reaches the inner hair cells; and the medial system, which originates in the ventral nucleus of the trapezoid body (VNTB) and innervates the OHCs. A previous study carried out in our laboratory showed that in congenitally hypothyroid animals, the neurons which give rise to the efferent system are normal in number and distribution, although smaller in size. The aim of the present work was to study the efferent fibers in the auditory receptor of hypothyroid animals, by means of stereotaxic injections of biotinylated dextran amine in the nuclei that give rise to the olivocochlear system: LSO and VNTB. In hypothyroid animals, injections in LSO gave rise to lateral olivocochlear fibers lacking their characteristic dense terminal arbors, while injections in the VNTB-labeled fibers terminating in the spiral bundle region, far from the OHCs with which they normally contact. In the latter case, only a small percentage of labeled fibers reached the OHCs area, giving off only two radial branches maximum. Because the number of neurons which develop into the efferent innervation was normal in hypothyroid animals, we conclude that medial fibers may contact a new target. Copyright 2003 Wiley-Liss, Inc.

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Year:  2003        PMID: 12687710     DOI: 10.1002/cne.10620

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


  4 in total

Review 1.  Making sense with thyroid hormone--the role of T(3) in auditory development.

Authors:  Lily Ng; Matthew W Kelley; Douglas Forrest
Journal:  Nat Rev Endocrinol       Date:  2013-03-26       Impact factor: 43.330

2.  Deafness and permanently reduced potassium channel gene expression and function in hypothyroid Pit1dw mutants.

Authors:  Mirna Mustapha; Qing Fang; Tzy-Wen Gong; David F Dolan; Yehoash Raphael; Sally A Camper; R Keith Duncan
Journal:  J Neurosci       Date:  2009-01-28       Impact factor: 6.167

3.  Developmental delays consistent with cochlear hypothyroidism contribute to failure to develop hearing in mice lacking Slc26a4/pendrin expression.

Authors:  Philine Wangemann; Hyoung-Mi Kim; Sara Billings; Kazuhiro Nakaya; Xiangming Li; Ruchira Singh; David S Sharlin; Douglas Forrest; Daniel C Marcus; Peying Fong
Journal:  Am J Physiol Renal Physiol       Date:  2009-08-19

4.  Genetic background of Prop1(df) mutants provides remarkable protection against hypothyroidism-induced hearing impairment.

Authors:  Qing Fang; Alicia M Giordimaina; David F Dolan; Sally A Camper; Mirna Mustapha
Journal:  J Assoc Res Otolaryngol       Date:  2011-12-06
  4 in total

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