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D R Trune

Publications and source records attributed to D R Trune.

At least 55 records · Page 3Linked to original sources
PubMed1988

Decreased protein synthesis in cochlear nucleus following developmental auditory deprivation. Use of vascular saline perfusion to improve small tissue sample analysis.

The incorporation of tritiated leucine was used as an index of protein synthesis in the cochlear nucleus (CN) of mice unilaterally (right side) hearing deprived throughout the period of hearing development. Right-left differences in radiolabel concentration were measured by scintillation counting of whole tissue homogenates. To improve upon the detection of small differences in radiolabel incorporation, the brain was perfused with saline prior to removal of CN tissue and the results compared with the standard nonperfusion method of tissue collection. Statistical analyses demonstrated the perfusion significantly reduced the acid soluble (unbound) label in CN without affecting the amount of protein bound label. Furthermore, a significant right side decrease in leucine incorporation was seen with the perfusion treatment, but not in the nonperfused treatment. This demonstrated that developmental auditory deprivation led to a decrease in protein synthesis at maturity. The results also demonstrated that mechanisms for leucine uptake were not impaired and the decrease in protein synthesis was not due to reduced availability of precursor amino acid. Thus, the use of saline perfusion prior to tissue collection facilitated the identification of protein synthesis differences that were unidentified by the traditional method.

Acoustic Stimulation↗
PubMed1988

Influence of developmental auditory deprivation on neuronal ultrastructure in the mouse anteroventral cochlear nucleus.

Developmental auditory deprivation caused mouse anteroventral cochlear nucleus neurons to have significantly fewer auditory nerve terminals and more non-auditory nerve terminals. This suggested that stimulation regulated the developmental arborization of auditory nerve terminals and competition for synaptic space. Intracellularly, mitochondria were smaller and darker in the deprived neurons and appeared less active metabolically. Interference with these neuronal processes may underlie the impaired development seen in auditory deprivation.

Afferent Pathways↗
PubMed1988

Stimulation-dependent development of neuronal cytoplasm in mouse cochlear nucleus.

The extent of neuronal development in the mouse ventral cochlear nucleus was examined in normal and developmentally auditory deprived mice. Mice were unilaterally deprived on postnatal day three by external auditory meatus removal and sacrificed with controls on day 45, which is after the developmental period. Light microscopic morphometry of neuronal nucleus and cytoplasm areas demonstrated that the normal spherical and globular cells were larger in their low frequency regions than in their high frequency regions. This size difference occurred mainly in the cytoplasm. Developmental deprivation reduced neuronal cytoplasm areas similarly in the high and low frequency regions of both neuronal types, but had no effect on the size of the neuronal nucleus. It was interpreted that cytoplasmic metabolic events are dependent on developmental levels of stimulation and high and low frequency regions normally are differentially stimulated. Furthermore, these stimulation-dependent cytoplasmic events are impaired by developmental hypostimulation, which retards neuronal metabolism and growth. No changes were observed in the cochlear nucleus contralateral to the deprived side, suggesting that compensatory changes, such as hypertrophy, did not occur.

Aging↗
PubMed1988

Histologic changes in selenite cortical cataract.

Massive cortical cataract was produced 15-30 days after a single injection of an overdose of sodium selenite into 14-day-old rats. Most of the cortical cataract appeared to be due to extensive liquefaction of cortical fibers. Water influx, following initial damage to the epithelium by selenium, and action of lens proteases were probable mechanisms for the extensive liquefaction. Remarkably, selenite cortical cataract spontaneously cleared after several months, restoring essentially normal cells to the epithelium and outer and mid-cortex. Major mechanisms for clearing probably involved: (1) removal of damaged proteins from the lens by extensive proteolysis; and (2) replacement of fibers by resumption of normal fibergenesis. The data emphasized the remarkable reparative potential of the lens, and indicated the usefulness of the selenite cortical cataract as a model to study such processes.

Animals↗
PubMed1986

Cytoarchitecture and saccular innervation of nucleus y in the mouse.

The cytoarchitecture and saccular innervation of the mouse nucleus y were investigated by using Golgi, Nissl, and myelin stains and anterograde axonal transport of horseradish peroxidase. Nucleus y was found to be a compact group of cells in a small fiber-free region dorsal to the restiform body. Qualitative and morphometric analyses showed that most (75%) of the nucleus y neurons could not be reliably subdivided into morphologic subgroups, but varied continuously in soma size (15-25 microns), shape (fusiform to stellate), and number of dendrites (two to four), and had sparsely branched dendrites with an average of 3 to 4 spines per 10 microns of length. Three groups of cells that were identified morphometrically accounted for 10% (type I: large stellate cells), 9% (type II: long-dendrite cells), and 6% (type III: elongated soma cells) of the y neurons. Vestibular nerve axons transporting horseradish peroxidase after injury at their origin in the saccular neuroepithelium were found to form a dense terminal meshwork that was virtually co-extensive with the cytoarchitectonic boundaries of nucleus y. Nucleus y was distinguished from the overlying infracerebellar nucleus on the basis of anatomical, cytoarchitectural, and hodological features.

Animals↗
PubMed1986

Paraphysectomy-induced stimulation of parathyroid glands in mature frogs (Rana catesbeiana): evidence for telencephalic regulation of parathyroid gland function.

The relationship of the paraphyseal-choroid plexus complex to parathyroid gland function was investigated in adult frogs. Light microscopy and morphometric analysis indicated that total parathyroid gland volume, cell volume and vascular volume doubled by 7-28 days after surgical removal of the paraphyseal-choroid plexus complex (paraphysectomy). This increase correlated with the appearance of large Golgi-associated vesicles, an increase in the apparent number of cytoplasmic dense-core granules, and PTH within the parenchymal cells as monitored by immunofluorescence. Twelve months after paraphysectomy, parathyroid glands became cystic with a central fluid-filled cavity surrounded by a stratified cuboidal cell layer. The parenchymal cells of cystic glands contained numerous cytoplasmic dense-core granules and were also positive for PTH. Radioimmunoassay of cystic parathyroid fluid indicated a PTH concentration of 2 micrograms/microliter; however, analysis by SDS-PAGE indicated a wide range of proteins in cystic fluid. The results of this study indicate that paraphysectomy induces stimulation of the parathyroid glands and suggest a role for the paraphyseal-choroid plexus complex in the regulation of amphibian parathyroid gland function.

Animals↗
PubMed1983

Influence of neonatal cochlear removal on the development of mouse cochlear nucleus. III. Its efferent projections to inferior colliculus.

In order to determine the transneuronal developmental influences of auditory deafferentation, the right cochleas, with the first order spiral ganglion neurons, were removed in 6-day-old mice to eliminate all peripheral input to the right cochlear nucleus (CN). At 45 days, some of the efferent projections of right CN in these unilaterally lesioned mice and their unoperated controls were identified by retrograde transport of horseradish peroxidase from the contralateral (left) inferior colliculus (IC). In both groups of animals, reaction product was observed in neurons of the right CN, contralateral to the injection, and no labeling was seen in the ipsilateral left CN in either group. Contralaterally labeled were the fusiform cells of dorsal CN, the globular cells of ventral CN, and neurons within the nucleus of the intermediate acoustic stria. Quantification revealed significantly fewer fusiform and globular cells labeled in the deafferented CN, whereas the number of labeled acoustic stria neurons was the same in both groups. Although the deafferented CN had 65.4% fewer labeled neurons, the proportions projecting to IC were similar in the two groups, 7.8%. Because of this significant reduction in the number of deafferented CN neurons projecting to the contralateral IC, it was concluded that the transneuronal effects of deafferentation would be to deprive or deafferent developing neurons within the higher auditory brainstem nuclei.

Animals↗
PubMed1983

The behavior and vestibular nuclear morphology of otoconia-deficient pallid mutant mice.

Pallid mutant mice with no otoconia in their gravity receptors were behaviorally tested and their vestibular nuclei measured to determine if this developmental sensory deprivation had any detrimental effect on central vestibular structure and function. This absence of otoconia was correlated with disorientation in water and absence of air righting reflexes. The inferior and superior vestibular nuclei were smaller than normal, but neurons within regions that receive direct gravity receptor input were smaller only unilaterally in medial vestibular nucleus. It was tentatively concluded that the sensory deprivation resulting from reduced gravity receptor input was responsible for the behavioral and central morphological abnormalities.

Animals↗
PubMed1982

Influence of neonatal cochlear removal on the development of mouse cochlear nucleus: I. Number, size, and density of its neurons.

Right cochleae were aspirated from 6-day-old mice to determine the influence of cochlear integrity on the development of cochlear nucleus (CN). At 45 days of age, cochlear destruction was confirmed histologically, and the CN of unilaterally deafferented and control animals were analyzed morphometrically. The molecular, fusiform, and polymorphic layers of deafferented dorsal CN were reduced in volume, and the polymorphic layer neurons were fewer, smaller, and less dense. The octopus and multipolar cells regions in deafferented ventral CN (VCN) were smaller, and their neurons were fewer, smaller, and more densely packed. The VCN globular and small spherical cell regions were also smaller with fewer, denser, but normal-sized neurons. There were fewer VCN large spherical cells, but no change was measured in their size. The granule cell regions throughout CN were also reduced in volume. Overall, CN was reduced to 46% of its normal size and 34% of its normal neuronal numbers. These results in the mouse show that deafferentation before the onset of hearing causes more severe CN changes than those reported after adult deafferentation in other mammals and support the theory of a critical period in development when presynaptic integrity is much more important for neuronal maturation than it is for maintenance after the neuron is mature. This suggests that any congenital pathology that compromises the sensorineural structures of the cochlea may cause severe structural and functional abnormalities in the maturing central auditory nuclei.

Animals↗
PubMed1982

Influence of neonatal cochlear removal on the development of mouse cochlear nucleus: II. Dendritic morphometry of its neurons.

Right cochleae were aspirated from 6-day-old mice to determine the influence of cochlear integrity on the dendritic development of neurons within cochlear nucleus (CN). At 45 days of age, cochlear destruction was confirmed histologically and the brains were stained by the Golgi-Cox method to permit dendritic morphometry in CN ipsilateral (deafferented) and contralateral (normal) to the neonatally lesioned cochleae. The dendritic field cross-sectional area of ventral CN bushy cells was reduced on the deafferented side, as was the total dendritic length of stellate cells throughout ventral and dorsal CN. The neonatal deafferentation had no statistically significant effect on the total dendritic length of those dorsal CN fusiform cells that developed. These dendritic changes are interpreted as lack of development due to the loss of auditory nerve afferents during a critical period of development and indicate that any congenital pathology that compromises the cochlear sensorineural structures may lead to central auditory abnormalities as well.

Animals↗
PubMed1982

Cochlear nuclear complex of mice.

Using serial sections stained with luxol fast blue-cresyl violet, the cochlear nuclei of CBA/J mice were parcellated into the same cytoarchitectonic areas and layers that Osen (1969) used in cats. Within the spherical cell areas, the distribution of Nissl substance is more reliable than soma shape in identifying the spherical cells. The area of large spherical cells is extremely small in CBA/J mice but does contain significantly larger neurons than the small spherical cell area. In Golgi preparations, bushy cells are found in all areas of the ventral cochlear nucleus except in the octopus cell area and granule cell layer. They are more numerous anteriorly than posteriorly and details of their morphology are quite variable. Stellate cells are found throughout the ventral cochlear nuclei but are present in greatest numbers in the multipolar cell area; they are rare in the large spherical cell area and octopus cell area. Because size, soma morphology, and dendritic arborization vary on a continuum rather than in discrete steps, we have not subcategorized these neurons. Octopus cells are restricted to the posterior, dorsomedial area of the ventral cochlear nucleus. In the central region of the dorsal cochlear nucleus, stellate cells abound and are categorized as vertical, elongate, or radiate cells. In the granule layer of the dorsal cochlear nucleus there are both fusiform and Purkinje-like neurons, so named because of their resemblance to cerebellar Purkinje cells. These Purkinje-like cells differ from fusiform cells in having 1) a smaller cell body, spherical in shape, 2) no basal dendrites, 3) a sagittal dendritic orientation, 4) elaborate dendritic branching, and 5) abundant dendritic spines.

Animals↗
PubMedDate not supplied

Inner ear pathology in the Palmerston North autoimmune strain mouse.

The Palmerston North autoimmune strain mouse is a model for spontaneous systemic lupus erythematosus. Inner ear structure and function were examined during the onset and progression of systemic autoimmune disease to identify potentially correlated auditory system pathology. The onset of systemic disease occurred at 4 to 5 months of age and was characterized by elevated serum immune complexes, cryoglobulins, and antinuclear antibodies. Coincident with the onset of autoimmune disease was degeneration of the apical turn stria vascularis and outer hair cells. These cochlear changes progressed basalward. At 10 months of age, auditory brainstem response thresholds were elevated and the stria vascularis area was measurably smaller throughout the cochlea. Immunohistochemical staining showed immunoglobulin G deposits within the organ of Corti, the vas spirale of the basilar membrane, the scala tympani, and marrow cavities of the bony otic capsule. These results suggest that cochlear pathology may be immune mediated in this mouse, which would make the strain suitable for the study of the mechanisms relating inner ear abnormalities and autoimmune disease.

Age Factors↗
PubMedDate not supplied

Ultrastructure of otic capsule sclerosis in Palmerston North autoimmune mice.

PURPOSE: Numerous temporal bone studies have reported a correlation between systemic autoimmune disease and osteogenic lesions within the inner ear. However, little is known of the cellular mechanisms that relate these two disease processes. The Palmerston North (PN) autoimmune strain mouse exhibits both spontaneous systemic autoimmune disease and otic capsule sclerotic lesions that are similar in many ways to those reported in humans. This suggests the PN mouse is a potential model in which to study the cellular events responsible for immune-related otic capsule lesions. Therefore, an evaluation of the fine structure of the PN modiolus was conducted to better understand these matrix changes of the inner ear. MATERIALS AND METHODS: Inner ears were collected from 15 PN mice at ages from 17 to 24 months and prepared for electron microscopy. The ears were ultrastructurally evaluated to characterize the lesions and their associated cytoarchitecture. RESULTS: The sclerotic lesions consisted of an electron-dense mass that appeared lobulated or layered, usually adjacent to the modiolar bone and blood vessels. Immediately surrounding the lesions were activated fibroblasts and fine fibrillar material in the extracellular space between them. The sclerotic foci often were apposed to normal modiolar bone that never appeared degraded. CONCLUSIONS: The similarities between these bony lesions and known human otic capsule diseases suggests parallel processes are involved. Thus, further study of the PN inner ear may provide insight into the cellular events that underlie otic capsule and other temporal bone alterations in systemic autoimmune diseases.

Animals↗
PubMedDate not supplied

The relative importance of head size, gender and age on the auditory brainstem response.

Correlations between the ABR (auditory brainstem response) and subject characteristics of gender, age, and head diameter were established in simple and multiple regression analyses of normal hearing individuals. The simple regression tests demonstrated that head diameter and gender were significantly correlated with the latencies and amplitudes of waves I, III, and V and the I-V and III-V interpeak intervals. In nearly all cases, head diameter correlated more highly with the ABR waves than did gender. Males had longer latencies than females with comparable head diameter, suggesting that factors other than head size are differentiating them. Age was significantly correlated only with the latency of wave III. All significant subject variables also were compared simultaneously in a multiple regression analysis to determine their order of significance and relative contributions to the ABR wave latencies. This permitted the establishment of regression equations for each wave latency to predict the ABR with measurable subject characteristics.

Adolescent↗
PubMedDate not supplied

Histochemical localization of carbonic anhydrase in the inner ear.

Carbonic anhydrase was histochemically located in chinchilla inner ear tissues. A strong carbonic anhydrase reaction was observed in the spiral ligament cells, Boettcher's cells, the external sulcus cells, and the stria vascularis (intermediate and/or basal cells). The enzymatic reaction was also positive in the supporting cells of all vestibular sensory epithelia, as well as in the dark cells and transitional cells of the utricle and saccule. Some epithelial cells of the endolymphatic sac were also positive. It is speculated that this enzyme may be involved in: 1) ionic or fluid regulation of the endolymph, 2) removal of CO2 from the inner ear tissue near the sensory cells, and 3) otoconia formation and maintenance.

Animals↗
PubMedDate not supplied

A morphometric study of the pallid mutant mouse inner ear.

Mice homozygous for the mutant gene pallid (pa/pa) often lack otoconia in some or all of their maculae and are used to study the influences of gravity receptor hypostimulation on vestibular-related behaviors. Since the value of this animal model is based on the assumption that the vestibular sensorineural elements are normal, a morphometric analysis was done on the inner ear of these otoconia-deficient mice to see whether sensori-neural structures are also affected by the pallid gene. In pallid mice lacking all otoconia, the sensory epithelia of the utricle, saccule, and semicircular canal cristae were the same size as in their heterozygous (pa/+) controls. Although the superior and inferior divisions of the vestibular ganglion of the pallid mice were smaller than normal, the first-order neurons within these divisions were normal in size, number, and density. However, the superior divisions in both groups had larger neurons than did the inferior divisions. Within the pallid cochlea, first-order auditory neurons within the spiral ganglion were smaller than normal, but the scala media was larger. Since the significant vestibular influences of the pallid gene are limited primarily to the otoconia, behavioral abnormalities reported for these otoconia-deficient mice are apparently due only to gravity receptor hypostimulation.

Animals↗