Ablation of inner hair cells by carboplatin alters cells in the medial K+ flow route and disrupts tectorial membrane

Citation
Ss. Spicer et al., Ablation of inner hair cells by carboplatin alters cells in the medial K+ flow route and disrupts tectorial membrane, HEARING RES, 136(1-2), 1999, pp. 139-150
Citations number
39
Categorie Soggetti
da verificare
Journal title
HEARING RESEARCH
ISSN journal
03785955 → ACNP
Volume
136
Issue
1-2
Year of publication
1999
Pages
139 - 150
Database
ISI
SICI code
0378-5955(199910)136:1-2<139:AOIHCB>2.0.ZU;2-Y
Abstract
The thesis that K+ effluxing from inner hair cells (IHCs) cycles medially b ack to endolymph through inner sulcus and interdental cells (IDCs) was test ed by comparing control chinchilla cochleas with those in which IHCs were s electively destroyed by carboplatin. By light microscopy inner sulcus cells appeared tall and nearly empty in control ears, but 4 months after the car boplatin treatment many showed vacuolization and shrinkage. Inner pillar ce lls also consistently developed abnormal vacuoles after carboplatin treatme nt. Control cochleas exhibited lateral columns and central clusters of IDCs which at their apex possessed expanded presumably hydrated phalanges. Four months after carboplatin, the IDC epithelium enclosed empty looking spaces and the apical phalangeal compartment collapsed into a thin, apparently de hydrated layer. This alteration was accompanied by changes in the tectorial membrane (TM) whereby the membrane's limbal zone thickened progressively t o form a tall hollow mound in advanced lesions. The clear spaces in the epi thelium and collapse of the phalanges are thought to reflect diminished flo w of ions and fluid through IDCs. The accumulation of limbal TM supports th e premise that IDCs secrete macromolecules for TM turnover as well as ions and fluid for promoting lateral migration of its precursor constituents. Oc curring after ablation of IHCs by carboplatin, the changes in inner pillar, inner sulcus and IDCs and limbal TM can be viewed as a secondary effect of the interrupted ion efflux from IHCs and as further evidence that this eff luent follows a medial route. (C) 1999 Elsevier Science B.V. All rights res erved.