Morphofunctional alterations in the olivocochlear efferent system of the genetic audiogenic seizure-prone hamster GASH:Sal.

The genetic audiogenic seizure hamster (GASH:Sal) is a model of a form of reflex epilepsy that is manifested as generalized tonic-clonic seizures induced by external acoustic stimulation. The morphofunctional alterations in the auditory system of the GASH:Sal that may contribute to seizure susceptibility have not been thoroughly determined. In this study, we analyzed the olivocochlear efferent system of the GASH:Sal from the organ of Corti, including outer and inner hair cells, to the olivocochlear neurons, including shell, lateral, and medial olivocochlear (LOC and MOC) neurons that innervate the cochlear receptor. To achieve this, we carried out a multi-technical approach that combined auditory hearing screenings, scanning electron microscopy, morphometric analysis of labeled LOC and MOC neurons after unilateral Fluoro-Gold injections into the cochlea, and 3D reconstruction of the lateral superior olive (LSO). Our results showed that the GASH:Sal exhibited higher auditory brain response (ABR) thresholds than their controls, as well as absence of distortion-product of otoacoustic emissions (DPOAEs) in a wide range of frequencies. The ABR and DPOAE results also showed differences between the left and right ears, indicating asymmetrical hearing alterations in the GASH:Sal. These alterations in the peripheral auditory activity correlated with morphological alterations. At the cochlear level, the scanning electron microscopy analysis showed marked distortions of the stereocilia from basal to apical cochlear turns in the GASH:Sal, which were not observed in the control hamsters. At the brainstem level, MOC, LOC, and shell neurons had reduced soma areas compared with control animals. This LOC neuron shrinkage contributed to reduction in the LSO volume of the GASH:Sal as shown in the 3D reconstruction analysis. Our study demonstrated that the morphofunctional alterations of the olivocochlear efferent system are innate components of the GASH:Sal, which might contribute to their susceptibility to audiogenic seizures. This article is part of a Special Issue entitled "Genetic and Reflex Epilepsies, Audiogenic Seizures and Strains: From Experimental Models to the Clinic".

The topical use of insulin accelerates the healing of traumatic tympanic membrane perforations.

OBJECTIVE: In recent years, there has been a tendency to search for regulatory substances that can optimize the healing process of perforated tympanic membranes (TMs). The purpose of this study was to determine the effects of using topical insulin on the healing process of traumatic TMs perforations. STUDY DESIGN: Experimental. METHODS: Tympanic membranes of 20 Wistar rats were perforated in two sections, anterior and posterior to the malleus. The rats were divided into two groups: control and insulin. The insulin group was treated with topical regular insulin. The TMs were histologically examined 3, 5, and 7 days after the perforation through a morphometric analysis of the epithelial layer thickness, perforation size, TM cross-sectional area, semiquantitative and qualitative evaluation of the collagen production by polarization microscopy, and immunohistochemical evaluation of epithelial cells and myofibroblasts markers. RESULTS: Insulin accelerated the healing process of the perforated TMs (P < 0.01); stimulated early thickening of the outer epithelial layer (P < 0.01); contributed to a larger identification of the antipankeratin antibody as epithelial marker (P < 0.05); and increased labeling of smooth muscle anti-alpha-actin antibody (P < 0.05), indicating greater proliferation of myofibroblasts. When the topical insulin was used, it resulted in a greater formation of collagen tissue (P < 0.05), with thicker and better-organized collagen fibers (P < 0.05). CONCLUSION: Insulin accelerated the healing process of TMs traumatic perforations.

Spontaneous healing of the tympanic membrane after traumatic perforation in rats.

UNLABELLED: The most common etiologies of tympanic membrane perforation are infections and trauma. OBJECTIVE: The objective of the present study was to assess the healing of traumatic tympanic membrane perforation in rats. METHODS: The tympanic membrane from male Wistar rats was perforated in the anterior and posterior portions to the handle of the malleus. Five tympanic membranes were evaluated 3 days after tympanic perforation; 5 after 5 days; 5 after 7 days; 3 after 10 days; and 4 after 14 days. The tympanic membranes were submitted to histopathological evaluation after hematoxylin-eosin staining. RESULTS: Tympanic membrane closure occurred at about 7-10 days after injury and the healing process was complete by day 14. The proliferative activity of the outer epithelial layer was present close to the handle of the malleus and to the tympanic annulus. CONCLUSION: The spontaneous healing process of the tympanic membrane starts from the outer epithelial layer, with later healing of the lamina propria and the mucosal layer.

Spontaneous healing of the tympanic membrane after traumatic perforation in rats / Cicatrização espontânea da membrana timpânica após sua perfuração traumática: estudo experimental em ratos,

OBJECTIVE: The objective of the present study was to assess the healing of traumatic tympanic membrane perforation in rats. METHODS: The tympanic membrane from male Wistar rats was perforated in the anterior and posterior portions to the handle of the malleus. Five tympanic membranes were evaluated 3 days after tympanic perforation; 5 after 5 days; 5 after 7 days; 3 after 10 days; and 4 after 14 days. The tympanic membranes were submitted to histopathological evaluation after hematoxylin-eosin staining. RESULTS: Tympanic membrane closure occurred at about 7-10 days after injury and the healing process was complete by day 14. The proliferative activity of the outer epithelial layer was present close to the handle of the malleus and to the tympanic annulus. CONCLUSION: The spontaneous healing process of the tympanic membrane starts from the outer epithelial layer, with later healing of the lamina propria and the mucosal layer. .

OBJETIVOS: Avaliar o reparo cicatricial de perfurações traumáticas da membrana timpânica em ratos. MÉTODO: A membrana timpânica de ratos Wistar machos foram perfuradas nas porções anterior e posterior ao cabo do martelo. Cinco membranas timpânicas foram avaliadas 3 dias após perfuração timpânica; 5 após 5 dias; 5 após 7 dias; 3 após 10 dias; e 4 após 14 dias. As membranas timpânicas foram submetidas à avaliação histopatológica após coloração com hematoxilina- eosina. RESULTADOS: O fechamento da membrana timpânica ocorreu em torno de 7 a 10 dias após perfuração traumática, e o processo de cicatrização estava completo no 14° dia. A atividade proliferativa da camada epitelial externa foi identificada próxima ao cabo do martelo e ao ânulus timpânico. CONCLUSÃO: O processo de cicatrização espontânea da membrana timpânica se inicia com a camada epitelial externa, com posterior cicatrização da lâmina própria e da camada mucosa. .