Properties and distribution of anterior VIIIth nerve excitatory inputs to the goldfish Mauthner cell.
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Mercury deposition and its relationship to the inner ear function in methylmercury-poisoned rats were examined. Rats were poisoned with methylmercury chloride. After the appearance of signs of poisoning, the cerebellar and inner ear tissues were examined histochemically using an autoradiographic procedure. Mercury deposits were typically found in the cerebellum and appeared in parts of the vestibular nerves, cochlear nerves, spiral ganglion and stria vascularis. In the vestibule, a slight mercury deposition was observed in the acoustic maculae and in the cochlea; only one instance of mercury deposit in the organ of Corti was detected. The effect of mercury on the inner ear function was also assessed on the basis of immunohistochemical localization of substance P which is believed to be a neurotransmitter in the inner ear. However, no pathological changes were detected. These findings suggest that methylmercury deposition has little effect on the inner ear function.
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It is very valuable for temporal bone morphologists to be able to recognize temporal bone serial sections in three dimensions and to be able to measure temporal bone structures three-dimensionally. We can now do 3-dimensional reconstruction to visualize the structures of vestibular endorgans (utricular and saccular maculae) and measure these endorgans in space by means of a small computer system and software that we developed. As well as obtaining the dimensions--such as length and area--of the utricular and saccular maculae, we also found that (1) most of the utricular macula lies in one plane, which is the same as the plane of the lateral semicircular canal, (2) the saccular macula is shaped like part of a sphere, and (3) the angle between the two maculae is less than a right angle. Such knowledge is indispensable to the evaluation of the function of the utricular and saccular maculae.
To investigate the origin of non-auditory fibres in the apical area of the avian cochlear ganglion, we recorded from nerve fibres in the young chick (87% of animals were aged between 5 and 10 days post-hatching). After characterization of their spontaneous activity patterns and, if present, their responses to sound, some fibres were stained with cobalt-ion injections and traced to their peripheral terminals. All stained fibres which were traced to the lagenar macula (N = 13) were non-auditory. They did not increase firing rate or phase-couple to sound stimuli. Their spontaneous activity was either regular (12 cases) or irregular (1 case). Regularly-firing cells all innervated several to very many hair cells, whereby there was no great difference in the pattern of spontaneous activity between those making calyx endings on relatively few hair cells in the striola region and those making small bouton endings on up to 80 hair cells outside the striola. All fibres that responded in any way to sound were irregularly spontaneously active. Three fibres, two of which only responded to sound with phase-coupling, innervated several hair cells in the apical, abneural region of the basilar papilla. Two other fibres traced to the basilar papilla are of previously undescribed types.
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The hair cell orientation of the macula lagenae in eels at three different stages of life was examined with the light microscope. Part of the posterior periphery of all three stages was occupied by a few rows of sensory cells having their kinocilium pointing in a direction opposite to the direction of the adjacent sensory cells. The width of this peripheral belt remained the same at all three stages of life, in spite of a considerable growth of the sensory epithelium, and the belt was always confined to the margin. This indicates an intraepithelial growth of at least part of the neuroepithelium of the lagenar macula of the European eel.
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The development of otoconia in the utricular and saccular maculae from initial embryonic formation to adult stages was examined in Japanese quails. Both the morphology and size of the otoconia were quantified at different developmental stages. It was observed that the otoconia were initially formed on embryologic stage E5 in the saccule and E6 in the utricle. Otolith mass areas increased in a sigmoidal growth pattern, with saccular otolith areas being smaller than the utricular mass areas. Saccular otolith masses reached adult values at embryonic stage E12 and utricular areas reached adult values at post-hatch day 7. Mature individual otoconia were characterized by a barrel shape with two trihedral faceted ends. However, initial formation of otoconia at E5 (saccular) and E6 (utricular) maculae was characterized by a double fluted morphology that consisted of an hourglass shape with extended fins forming trihedral angles of 120 degrees. Double fluted otoconia rapidly filled, so that by embryonic day 8 mature otoconia dominated the maculae for the remainder of development through adulthood. Thus, a progression from double fluted to mature forms was noted. Mature utricular otoconia in adult quails averaged 11 microm in length and 5 microm in width, with length/width ratios of approximately 2.5:1, for all size ranges. Saccular otoconia were smaller, having about 70% the size of utricular otoconia in both length and width. During development, the average size and range of individual otoconia increased nearly linearly for both otolith organs. In the utricular macula, large otoconia were concentrated in the lateral regions of the epithelium. In contrast, otoconia of various sizes were distributed uniformly across the surface of the saccular macula.
In humans, metastatic tumors which invaded the temporal bones have been studied in regard to the relationship between histopathologic findings and clinical symptoms. On the other hand, there is no experimental study using an animal model for tumor infiltration into the temporal bone. This study was designed to establish such an animal model and examine the temporal bones histopathologically. Rat thymic lymphoma cell (FTL-A2) were inoculated into the cisterna magna of Wistar rats. The animals were decapitated under deep anesthesia with pentobarbital sodium from the 1st to 8th day after inoculation. Their heads were fixed with Heiden-hain SuSa solution, decalcified, dehydrated, embedded in celloidin, and sectioned horizontally at a thickness of 25 microns. These were stained with hematoxylin and eosin, and histologically examined by light microscopy. Inoculated tumor cells showed active viability in the arachnoid space at a rate of 98%. Two major routes of tumor cell infiltration into the inner ear were found: the cochlear aqueduct and the internal auditory canal. At the early stage after the inoculation, tumor cells infiltrated the scala tympani through the cochlear aqueduct. Invading the fiber of the cochlear nerve, tumor cells infiltrated Rosenthal's canal via the tractus spiralis foraminosus, and passed through Rosenthal's canal and the osseous spiral lamina into the scala tymani. However, tumor cells did not infiltrate the organ of Corti through the habenula perporata. Tractus spiralis foraminosus and habenula perforata functioned as a barrier against tumor infiltration. In a few cases, tumor cells infiltrated over the macula cribrosa into the subepithelial space of the utricule and saccule. The macula cribrosa functioned as a barrier.