References: Hair growth and hair loss
Audiol Neurootol. 2004 Mar-Apr;9(2):88-106.
Hearing loss in athyroid pax8 knockout mice and effects of thyroxine substitution.
Christ S, Biebel UW, Hoidis S, Friedrichsen S, Bauer K, Smolders JW.
Max-Planck-Institut fur experimentelle Endokrinologie, Hannover, Germany.
Pax8-/- mice do not develop thyroid follicular structures and thus provide an ideal animal model to study the consequences of congenital hypothyroidism. Despite their athyroidism, Pax8-/- mice survive up to postnatal day 21 (P21). No auditory brain stem responses (ABR) to sound could be recorded in these animals at 130 dB SPL, even at P21, when hearing reaches adult sensitivity in control mice. Abnormalities in the outer and middle ear structures were found in a considerable percentage of Pax8-/- animals. Maturation of the inner ear appeared delayed by about 1 week with respect to euthyroid controls. Hearing of adult Pax8-/- mice could be nearly normalized by early postnatal substitution with thyroxine (T(4)), but structural and functional restoration of hearing was incomplete. Even when T(4) substitution was initiated at P1, ABR thresholds, measured at 6 weeks of age or more, were increased by about 20 dB, and each day of delay in the start of T(4) substitution resulted in an additional threshold loss of about 4 dB. The most prominent structural deficit in Pax8-/- animals in which T(4) substitution was started at P8 or later was an abnormally thick tectorial membrane. In these late-substituted animals, disarray of stereovilli from inner and outer hair cells was observed and also outer hair cell loss was found, predominantly in the basal part of the cochlea. The degree of structural disorder increased the later T(4) substitution was initiated. The structural and functional consequences of postnatal athyroidism observed in Pax8-/- mice are largely in agreement with and extend those data obtained from hypothyroid animal models in which hypothyroidism was induced by goitrogenic agents (methimazole, propylthiouracil) or animal models with disrupted genes for the TSH receptor or the thyroid hormone receptors. The hearing loss and also the recovery effect by T(4) substitution in Pax8-/- mice is larger than that in the other models. Although Pax8-/- mice are born by euthyroid Pax8+/- dams, the Pax8-/- phenotype could not be completely restored by immediate postnatal T(4) substitution, indicating that some deficits are the consequence of prenatal T(4) deficiency of the offspring. Copyright 2004 S. Karger AG, Basel
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14981357&dopt=Abstract [PubMed - in process]
Laryngoscope. 1992 Jun;102(6):693-703.
Neural regeneration in the noise-damaged chinchilla cochlea.
Bohne BA, Harding GW.
Department of Otolaryngology, Washington University School of Medicine, St. Louis, MO 63110.
Recent studies in the bird ear have shown that degenerated hair cells are sometimes replaced by regenerated receptor cells. The present study evaluated the adult mammalian cochlea for evidence of hair-cell and nerve-fiber regeneration. Eighty-eight noise-damaged chinchilla cochleas were examined as plastic-embedded whole mounts by phase-contrast and bright-field microscopy. No signs of hair-cell regeneration were found. However, 32 (70%) of 46 cochleas damaged by high-intensity noise and 20 (48%) of 42 cochleas damaged by moderate-intensity noise contained a variable number of nerve fibers which appeared to be regenerated. These fibers, which were located in severely damaged areas of organ of Corti, differed from residual fibers with respect to their diameters, the degree and pattern of myelination, and by the abnormal paths they followed within the osseous spiral lamina and on the basilar membrane. The number of regenerated fibers varied with type of exposure and length of recovery. The strongest response was found in ears exposed to a high-intensity, low-frequency noise. The results described here indicate that a potential exists for the biological restoration of the mammalian inner ear.
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1602919&dopt=Abstract
Hear Res. 1992 Apr;59(1):46-58.
Hair cell regeneration in the adult budgerigar after kanamycin ototoxicity.
Hashino E, Tanaka Y, Salvi RJ, Sokabe M.
Hearing Research Laboratories, State University of New York, Buffalo 14214.
Adult budgerigars were given kanamycin at a dose of 200 mg/kg/day for 10 successive days. At 1, 7, 14 and 28 days after the drug treatment, the cochleae of the birds were processed for scanning electron microscopy (SEM). Complete degeneration of sensory hair cells was observed in the basal 55-75% of the basilar papilla immediately after the treatment. Regenerating hair cells, characterized by clusters of microvilli and small apical surfaces, were present in the basal end of the papilla as early as one day post-treatment. During the 28 day recovery period, the number of hair cells progressively increased beginning at the base and spreading toward the apex. Although the appearance of the basilar papilla had improved considerably by 28 days post-treatment, the sensory epithelium still contained a number of pathologies, most noticeably, incomplete restoration of hair cell number in the most apical part of the damaged region and the disorganization of hair cell packing. These remaining pathologies may be responsible for the permanent threshold shifts observed in budgerigars exposed to the same dose of kanamycin treatment (Hashino and Sokabe, 1989).
online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1629046&dopt=Abstract
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