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Biomedical subjects

D B Webster

Publications and source records attributed to D B Webster.

At least 55 records · Page 3Linked to original sources
PubMed1975

Auditory systems of Heteromyidae: postnatal development of the ear of Dipodomys merriami.

Serial histological sections of kangaroo rats of postnatal ages 0-, 3-, 7-, 10-, and 14-days were prepared and studied. At birth the middle ear is mostly filled with mesenchyme and small in size, having only a small hypotympanum and a very small epitympanic recess. During the first postnatal two weeks, much of the hypertrophy found in the adult middle ear develops. Because an entotympanic element is nev er formed, the previously called entotympanic chamber is here renamed the hypotympanum. The epitympanic recess greatly expands to form what has been called the dorsal (or anterior) mastoid sinus. Since this chamber has no relation to the mastoid, it is here renamed the epitympanum. Posteriorly, the previously called posterior mastoid sinus develops from the growth of the hypotympanum into and beyond the region of the posterior and horizontal semicircular canals. In development and adult position it is comparable to the primate antrum and so is here renamed the antrum. At birth the organ of Corti is very immature but its major cell types can be identified. During the first two weeks of development the following events occur: (1) the vas spirale disappears, (2) the inner spiral sulcus cells atrophy, (3) the hair cells and supporting cells mature, (4) the cells of Hensen differentiate with their apical processes elevating the reticular lamina, (5) the innermost cell of Claudius migrates under and supports the Hensen's cells, and (6) the hyaline mass of the zona pectinata of the basilar membrane loses its connective tissue cells and expands in size. The developmental events support the previous description and identification of Hensen's and Claudius' cells.

Age Factors↗
PubMed1975

Projections of the trapezoid body and the superior olivary complex of the Kangaroo rat (Dipodomys merriami).

Glass micropipettes filled with 2 M sodium cyanide were used to physiologically locate and iontophoretically damage the nucleus of the trapezoid body (NTB), the medial superior olive (MSO), and the lateral superior olive (LSO). Mechanical lesions were made in the trapezoid body as it leaves the cochlear nuclei. After a 3- to 10-day survival time the projections and terminal degeneration were traced with the Fink-Heimer and Nauta-Gygax stains. The ventral cochlear nucleus (VCN) projects via the trapezoid body to ipsilateral LSO, ipsilateral preolivary nuclei, ipsilateral lateral and a contralateral medial dendritic fields of MSO, and contralateral NTB; there is also a small ipsilateral projection to the ventral nucleus of the lateral lemniscus (VNLL) and the central nucleus of the inferior colliculus (CNIC). Some trapezoid body fibers ascend via the contralateral lateral lemniscus to VNLL, DNLL (dorsal nucleus of the lateral lemniscus), and CNIC. There is no projection from the ventral cochlear nucleus to the ipsilateral NTB and contralateral preolivary nuclei. All portions of NTB project ipsilaterally to LSO (ventral NTB to dorsomedial LSO, dorsal NTB to ventral LSO) and to the retro-olivary nucleus. In two animals with NTB lesions there is also degeneration in the ventromedial portion of the ipsilateral facial nucleus. NTB projects contralaterally by way of the stria of Monakow to the pyramidal and molecular cell layers of the dorsal cochlear nucleus (DCN). The NTB does not project ipsilaterally to MSO, preolivary nuclei, VNLL, DNLL and CNIC. Contralaterally there are no projections to any of the nuclei of the auditory pathway except the DCN. Most MSO projections are ipsilateral. The densest goes by way of the lateral lemniscus to the lateral aspect of the ipsilateral CNIC, terminating throughout its dorsoventral axis. MSO also projects bilaterally to the pyramidal and molecular cell layers of dorsal cochlear nucleus (DCN), and ipsilaterally to the ventral portion of the motor nucleus of V and to the facial nucleus. MSO does not project ipsilaterally to the LSO, NTB, preolivary, VCN and retro-olivary nuclei. On the contralateral side, all structures except the DCN are free of projection patterns from axons originating in the MSO. LSO projects bilaterally to the central and ventral portions of CNIC and to the nuclei of the lateral lemnisci, and ipsilaterally to the large and small spherical cell areas of anterior ventral cochlear nucleus (AVCN) and to all portions of DCN. The LSO does not project ipsilaterally to the NTB, MSO, preolivary and retro-olivary nuclei. On the side opposite, this nucleus does not project to NTB, MSO, retro-olive, VCN, preolivary and LSO. For all lesions regardless of the site, there is no degeneration found rostral to the CNIC. The medial geniculate body or other structures in the diencephalon or cortex are free of any fields of terminal degeneration.

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PubMed1975

The effects of cosmic particle radiation on pocket mice aboard Apollo XVII: X. Results of ear examination.

In the five pocket mice flown on Apollo XVII, no evidence was found that the inner ear had been damaged, though poor fixation precluded detailed study. On the other hand, the middle ear cavity was involved in all the mice, hemorrhage having occurrred in response to excursions in pressure within the canister that housed the mice during their flight. The same occurred in flight control mice which had been subjected to pressure excursions of much the same magnitude. A greater degree of exudation into air cells and greater leukotaxis were noted in the flight animals than in the control animals. There was no increase in leukocyte population along the paths of the 23 cosmic ray particles registered in the subscalp dosimeters that traversed the middle ear cavities of the flight mice. The increased exudation and the greater response by leukocytes in the flight mice may have been causally related to the lesions found in their olfactory mucosa but there were no data in support of this possibility.

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PubMedDate not supplied

Conductive hearing loss affects the growth of the cochlear nuclei over an extended period of time.

During normal growth in CBA/J mice, the volume of dorsal and ventral cochlear nuclei change very little between 1 and 3 days of age; then more than double between 6 and 12 days of age. After 12 days, the rate of growth declines, but growth continues through at least 90 days. The globular cells of the ventral cochlear nucleus also double their soma areas between 6 and 12 days, but then grow no more. The number of ventral cochlear nucleus neurons containing Nissl substance doubles between 6 and 12 days of age and then remains stable. This increase in neuronal numbers is probably caused by differentiation of neuroblasts into neurons, not by mitoses. Conductive losses from 4 to 45 days, and from 24 to 45 days, both result in reduced volume of the ventral cochlear nucleus, but have no effect on the volume of the dorsal cochlear nucleus. Globular cell area is affected by a conductive loss from 4 to 45 days of age, but not by a conductive loss from 24 to 45 days. Therefore, conductive losses affect neuropil growth beyond the time when soma size is no longer affected by these losses.

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PubMedDate not supplied

Sound amplification negates central effects of a neonatal conductive hearing loss.

Neonatal CBA/J mice with external auditory meati removed were raised in a sound-amplified environment. If amplification continued until sacrifice at 24 or 45 days of age, both cochlear nuclear volumes and cross-sectional areas of VCN globular cells were of normal size; without amplification both measurements were significantly reduced.

Acoustic Stimulation↗
PubMedDate not supplied

Effects of neonatal conductive hearing loss on brain stem auditory nuclei.

Both postnatal auditory deprivation and experimentally produced conductive hearing losses in mice result in incomplete maturation of most brain stem auditory neurons. The affected groups are: octopus cell, globular cell, small spherical cell, and large spherical cell groups in ventral cochlear nuclei; and the lateral superior olive and medial nucleus of the trapezoid body of the superior olivary complex. When 45 days of auditory deprivation are followed by 45 days of normal acoustic stimulation, there is incomplete maturation of neurons in: multipolar cell, globular cell, small spherical cell, and large spherical cell groups in ventral cochlear nuclei; lateral superior olive and medial nucleus of trapezoid body in superior olivary complex; and central nucleus of inferior colliculus. A critical period exists when adequate sound stimulation is needed for full development of these neurons.

Acoustic Stimulation↗
PubMedDate not supplied

Brainstem histopathology following chronic scala tympani implantation in monkeys.

Degeneration in brainstem auditory nuclei was studied in monkeys following chronic implantation with scala tympani multielectrode systems. Nauta and Fink/Heimer-stained material from animals with survival times to 16 months were studied. The density and distribution of degeneration in the cochlear nuclei were consistent with observed patterns of spiral ganglion cell degeneration. Transneuronal degeneration was seen up to the level of the inferior colliculus. The density and form of the degeneration material in animals of varying survival times was consistent with the interpretation that a process of continuing degeneration occurred in these implanted ears.

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PubMedDate not supplied

Mouse brainstem auditory nuclei development.

The cross-sectional areas of brainstem auditory neurons were measured in a potential developmental series of mice. There is no demonstrable neuronal growth between days 1 and 3. Between days 3 and 12 the neuronal somas grow rapidly to their adult size. Most of this growth occurs prior to any cochlear physiological activity and all of it occurs before cochlear maturation. Most brainstem auditory neurons of 45-day-old mice postnatally deprived of sound or with conductive losses are of a size comparable to normal nine-day-old mice.

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