Distinct thyroid hormone-dependent expression of trkB and p75NGFR in nonneuronal cells during the critical TH-dependent period of the cochlea

Knipper, Marlies; Gestwa, Lika; Cate, Wouter‐Jan Ten; Lautermann, J.; Brugger, Heribert; Maier, Hannes; Zimmermann, Ulrike; Rohbock, Karin; Köpschall, Iris; Wiechers, B Ludlow; Zenner, Hans‐Peter

doi:10.1002/(sici)1097-4695(19990215)38:3<338::aid-neu4>3.0.co;2-1

Cited by 55 publications

(30 citation statements)

References 89 publications

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“…In the adult, both sulci are comprised of a monolayer of large cuboidal epithelial cells that appear largely unremarkable. While the cytologic changes that occur during outer sulcus formation have not been studied extensively, remodeling of the inner sulcus cells has been shown to be dependent on thyroid-hormone mediated expression of p75 ntr leading to cellular apoptosis (Knipper et al, 1999). Elimination of a large percentage of the cells within the developing inner sulcus is consistent with the observation that this region of the cochlear duct contains a large number of cells in the embryo.…”

Section: Kolliker's Organ and The Greater Epithelial Ridgesupporting

confidence: 56%

Cellular commitment and differentiation in the organ of Corti

Kelley¹

2007

Int. J. Dev. Biol.

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The organ of Corti, the sensory epithelium of the mammalian cochlea, develops from a subset of cells located along the dorsal side (referred to as the floor) of the cochlear duct. Over the course of embryonic development, cells within the developing organ of Corti become committed to develop as each of the unique cell types within the organ, including inner and outer hair cells, and at least four different types of supporting cells. Moreover, these different cell types are subsequently arranged into a highly rigorous cellular mosaic that includes the formation of ordered rows of both hair cells and supporting cells. The events that regulate both the location of the organ of Corti within the cochlear duct, the specification of each cell type and cellular patterning remain poorly understood. However, recent results have significantly improved our understanding of the molecular, genetic and cellular factors that mediate some of the decisions required for the development of this structure. In this review I will present an overview of cochlear development and then discuss some of the most recent and enlightening results regarding the molecular mechanism underlying the formation of this remarkable structure.

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Section: Kolliker's Organ and The Greater Epithelial Ridgesupporting

confidence: 56%

Cellular commitment and differentiation in the organ of Corti

Kelley¹

2007

Int. J. Dev. Biol.

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“…The presence of T3 only from the onset of thyroid gland activity at E17 up to P12 (B, red curve 3, squares), leads to normal hearing thresholds (A, bar 3) that is not different from hearing thresholds in untreated animals (A, bar 4) with a typically higher saturating plasma-T3 level (B, line 4, diamonds). Lower levels of plasma-T3 between P1 and P7 (B, curve 2, circle) similar to total decline of plasma-T3 levels (B, curve 1, circle) failed to generate normal hearing function (A, bar 1 and 2) (see also Knipper et al 1999). TH-deficient periods between the onset of thyroid gland function at E17 and P12 were induced by delaying fetal elevation in plasma-TH levels from E17 on indicated days postnatal E17 using MMI.…”

Section: Novel Th-dependent Processes In the Auditory System That Do mentioning

confidence: 90%

Thyroid Hormone Deficiency Before the Onset of Hearing Causes Irreversible Damage to Peripheral and Central Auditory Systems

Knipper

Zinn

Maier

et al. 2000

Journal of Neurophysiology

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169

156

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Thyroid hormone deficiency before the onset of hearing causes irreversible damage to peripheral and central auditory systems. J. Neurophysiol. 83: 3101-3112, 2000. Both a genetic or acquired neonatal thyroid hormone (TH) deficiency may result in a profound mental disability that is often accompanied by deafness. The existence of various TH-sensitive periods during inner ear development and general success of delayed, corrective TH treatment was investigated by treating pregnant and lactating rats with the goitrogen methimazole (MMI). We observed that for the establishment of normal hearing ability, maternal TH, before fetal thyroid gland function on estrus days 17-18, is obviously not required. Within a crucial time between the onset of fetal thyroid gland function and the onset of hearing at postnatal day 12 (P12), any postponement in the rise of TH-plasma levels, as can be brought about by treating lactating mothers with MMI, leads to permanent hearing defects of the adult offspring. The severity of hearing defects that were measured in 3-to 9-mo-old offspring could be increased with each additional day of TH deficiency during this critical period. Unexpectedly, the active cochlear process, assayed by distortion product otoacoustic emissions (DPOAE) measurements, and speed of auditory brain stem responses, which both until now were not thought to be controlled by TH, proved to be TH-dependent processes that were damaged by a delay of TH supply within this critical time. In contrast, no significant differences in the gross morphology and innervation of the organ of Corti or myelin gene expression in the auditory system, detected as myelin basic protein (MBP) and proteolipid protein (PLP) mRNA using Northern blot approach, were observed when TH supply was delayed for few days. These classical TH-dependent processes, however, were damaged when TH supply was delayed for several weeks. These surprising results may suggest the existence of different TH-dependent processes in the auditory system: those that respond to corrective TH supply (e.g., innervation and morphogenesis of the organ of Corti) and those that do not, but require T3 activity during a very tight time window (e.g., active cochlear process, central processes).

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“…Es zeigte sich, dass der Entzug von TH zwischen E3 und E17 (Knipper et al 1999) oder nach P12 (Abbildung 5; Knipper et al 2000) ohne Einfluss auf die Hörfunktion bleibt. Das heißt, weder mütterliches TH, noch eigenes TH nach Hörfunktionsbeginn, ist für die Entwicklung einer normalen adulten Hörfunk-tion essentiell; TH wird offenbar ausschließlich zwischen E17 und P12, in der kritischen Entwicklungsperiode vor Hör-funktionsbeginn benötigt, interessanterweise genau der Periode, in der sich bevorzugt genetisch bedingte und erworbene Innenohrdefekte manifestieren.…”

Section: Wann Beeinflusst Th Das Innenohr?unclassified

“…Eine ausbleibende morphogenetische Umgestaltung des Cortischen Organs bei Hypothyreose kann also durch TH-Gaben nach Hörfunktionsbeginn kompensiert werden. Wir lernten, dass weder das Ausbleiben der morphogenetischen Umgestaltung, eine fehlgesteuerte neuronalen Reorganisation (Knipper et al 1999(Knipper et al , 2000, noch eine verzögerte Myelinexpression (Knipper et al 1998) Michna et al 2003;Rüttiger et al 2003) weisen nicht nur auf die Notwendigkeit der Expression dieser Ionenkanäle für die Entwicklung einer normalen Hörfunkti-on hin, sondern deuten auch auf die Funktion dieser Kanäle für einen -durch spontane neuronale Aktivität kontrollierten -Reifungsprozess (Kros et al 1998;Marcotti et al 1999;Beutner und Moser 2001;Glowatzki und Fuchs 2002). In Analogie zu Reifungsprozessen in retino-geniculaten Verknüpfungen des visuellen Systems (Cabelli et al 1995), scheint die Spontanaktivität der IHZ durch eine efferente cholinerge negative Rückkopplungsschleife moduliert zu werden (Kros et al 1998;Glowatzki und Fuchs 2002;Marcotti et al 2003).…”

Section: Wie Können Kurze Th-mangelperioden Zu Schwerhörigkeit Und Taunclassified

“…Im immaturen Organ, gezeigt für P4 (Abbildung 8A), aber auch in Abwesenheit von TH, innervieren afferente Typ I Neurone ÄHZ und IHZ (Abbildung 8A). Efferenzen aus dem medialen oberen Olivenkomplex (MOC) des Stammhirns formen axosomatische Kontakte mit den IHZ (Abbildung 8A; Simmons 1992; Henley und Ryback 1995; Knipper et al 1999;Wiechers et al 1999 (Uziel et al 1985a, b;Knipper et al 1999), sondern auch die zeitgleich zur Reorganisation stattfindende Differenzierung der Schwann'schen Zellen wird massiv durch TH beeinflusst (Abbildung 8; Knipper et al 1998). MBP (myelin basic protein) und P0 (protein zero) (Lees und Brostoff 1984;Lemke 1995) werden nur in Anwesenheit von TH rechtzeitig vor Hörfunktionsbeginn hochreguliert (Knipper et al 1998).…”

Section: Wie Können Kurze Th-mangelperioden Zu Schwerhörigkeit Und Taunclassified

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Fire & Flower in the Cochlea oder Wie die Haarsinneszellen im Innenohr in Abhängigkeit von Thyroidhormon erblühen

Fraenzer¹,

Zimmermann²,

Weber³

et al. 2003

E-Neuroforum

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ZusammenfassungIn der kritischen Entwicklungsperiode des Innenohres, die mit dem Beginn der Hör-funktion endet -im Menschen ungefähr zwischen der zehnten und zwanzigsten embryonalen Woche, in Nagetieren wie Ratte und Maus zwischen Geburt und postnatalem Tag AbstractThyroid hormone dependence of the mammalian inner ear. During a critical developmental time period of the inner ear the immature organ of Corti develops to an adult functional organ upon synchronised morphological, cellular and neuronal processes. This period, which ends with the onset of hearing function, occurs in humans between the embryonal week (EW) 10 to ~20 and in rodents as mice and rats between birth and postnatal day 12 (P12). It is within this period when most of the acquired or genetic hearing deficits are manifested. Since decades it is known that thyroid hormone (TH) deficiency during pregnancy can lead to deafness, mental retardation and dwarfed growth (cretinism). However, the molecular basis of causing deafness upon hypothyroidism is not well understood in detail. Surprisingly, we learned that the thyroid hormone is necessary exclusively in the brief critical time period prior to the onset of hearing. We were able to see that TH obviously effects explicitly final differentiation processes step by step beginning from the periphery towards the cortex via transcriptional stimulation as well as suppression of genes. The identification of the genes regulated by TH, as well as the finding of their regulatory elements and their downstream following signalling cascades, should enable us to define potential causes for congenital and acquired deafness.

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Distinct thyroid hormone-dependent expression of trkB and p75NGFR in nonneuronal cells during the critical TH-dependent period of the cochlea

Cited by 55 publications

References 89 publications

Cellular commitment and differentiation in the organ of Corti

Cellular commitment and differentiation in the organ of Corti

Thyroid Hormone Deficiency Before the Onset of Hearing Causes Irreversible Damage to Peripheral and Central Auditory Systems

Fire & Flower in the Cochlea oder Wie die Haarsinneszellen im Innenohr in Abhängigkeit von Thyroidhormon erblühen

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