Thyroid hormone affects Schwann cell and oligodendrocyte gene expression at the glial transition zone of the VIIIth nerve prior to cochlea function

Abstract

All cranial nerves, as well as the VIIIth nerve which invades the cochlea, have a proximal end in which myelin is formed by Schwann cells and a distal end which is surrounded by oligodendrocytes. The question which arises in this context is whether peripheral and central parts of these nerves myelinate simultaneously or subsequently and whether the myelination of either of the parts occurs simultaneously at the onset of the cochlea function and under the control of neuronal activity. In the present paper, we examined the relative time course of the myelinogenesis of the distal part of the VIIIth nerve by analyzing the expression of peripheral protein P0, proteolipid protein and myelin basic protein. To our surprise, we observed that the expression of myelin markers in the peripheral and central part of the intradural part of the VIIIth nerve started simultaneously, from postnatal day 2 onwards, long before the onset of cochlea function. The expression rapidly achieved saturation levels on the approach to postnatal day 12, the day on which the cochlea function commenced. Because of its importance for the neuronal and morphological maturation of the cochlea during this time, an additional role of thyroid hormone in cochlear myelinogenesis was considered. Indeed, it transpires that this hormone ensures the rapid accomplishment of glial gene expression, not only in the central but also in the peripheral part of the cochlea. Furthermore, an analysis of the thyroid hormone receptors, TRaplha and TRbeta, indicates that TRbeta is necessary for myelinogenesis of the VIIIth nerve. Rapid thyroid hormone-dependent saturation of myelin marker gene expression in Schwann cells and oligodendrocytes of the VIIIth nerve may guarantee nerve conduction and synchronized impulse transmission at the onset of hearing. The thyroid hormone-dependent commencement of nerve conduction is discussed in connection with the patterning refinement of central auditory pathways and the acquisition of deafness.

A disease-associated mutation in thyroid hormone receptor α1 causes hearing loss and sensory hair cell patterning defects in mice

“…In the mouse cochlea, myelination by Schwann cells starts near birth at the cell bodies of SGNs and progresses to the central and peripheral processes between P8 and P10, just before the onset of hearing ( 65 ). It has been proposed that TRβ is necessary for myelinogenesis of the auditory nerve ( 66 ). In this study, we demonstrated a thickening of the myelin sheath in myelinated ANFs in 1-month-old Thra S1/+ mice.…”

Thyroxine Regulates the Opening of the Organ of Corti through Affecting P-Cadherin and Acetylated Microtubule

“…Thyroxine affects the development of the nervous system [ 25 ], which is also critical to the development of the inner ear. Early studies reported that the location and function of microtubules could be impacted by F-actin, and the microfilaments could be raised by the intracellular segments of adhesion molecules [ 26 , 27 ]. Thyroxine affects formation of the cytoskeleton, nerve regeneration and degradation of adhesion molecules in the testis [ 28 , 29 ], which indicates that thyroxine plays a similar role in the maturation of the OC.…”

Autoimmune thyroiditis in patients with sudden sensorineural hearing loss

“…Thyroid is the largest endocrine organ in the human body, and it secretes thyroid hormone, which is necessary to maintain the normal metabolism of the human body and can promote protein synthesis and regulate the metabolism of sugar, fat, water, salt, and vitamins. In addition, thyroid hormones play an important role in the development and maturation of spiral ganglion cells, hair cells, and hearing, formation of nerve myelin, oxygenation, and metabolism of Corti and stria vascularis 10–16 . Hyperthyroidism and hypothyroidism both can affect hearing, such as an increase change in wave V latency in the auditory brainstem response (ABR) and higher audiometric thresholds and TOAEs abnormality 17–19 …”

“…In addition, thyroid hormones play an important role in the development and maturation of spiral ganglion cells, hair cells, and hearing, formation of nerve myelin, oxygenation, and metabolism of Corti and stria vascularis. [10][11][12][13][14][15][16] Hyperthyroidism and hypothyroidism both can affect hearing, such as an increase change in wave V latency in the auditory brainstem response (ABR) and higher audiometric thresholds and TOAEs abnormality. [17][18][19] Hashimoto's thyroiditis, with an incidence of 0.3-1.5 cases per 1000 people, is characterized by increased thyroid volume, lymphocyte infiltration of parenchyma, and antibodies specific to thyroid antigens.…”