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Biomedical subjects

G R Bock

Publications and source records attributed to G R Bock.

45 records · Page 3Linked to original sources
PubMedDate not supplied

Developmental changes of susceptibility to auditory fatigue in young hamsters.

Susceptibility to auditory fatigue was studied in young hamsters by using an evoked-potential criterion of sound-induced threshold shift. Animals aged 15, 28, 40, 54 and 85 days were anesthetized and stimulated with a continuous tone (3 kHz, 110 dB SPL) for 10 min. Threshold shifts 1 min post-exposure were highest in animals aged 40 days, and lowest in animals aged 15 or 85 days. Threshold shifts recovered within 100 min in 15- and 85-day-old animals, but required considerably longer to recover in the other age-groups. The data suggest that young hamsters pass through a critical period of susceptibility to auditory fatigue. Comparison of this critical period with various indices of the development of hearing in the hamster suggests that the developmental events underlying the critical period do not occur in the middle ear.

Acoustic Stimulation↗
PubMedDate not supplied

The quivering mutant mouse: hereditary deafness of central origin.

Mice homozygous for the recessive quivering gene are largely unresponsive to sound, although their cochleas appear normal by light microscopy and cochlear hair cells do not degenerate with age. Cochlear potentials and inferior colliculus evoked responses were recorded in quivering mice (qv/qv) and in littermate controls (+/qv or +/+). There were no significant differences between mutants and controls in cochlear microphonic amplitudes or compound action potential thresholds, amplitudes and latencies. However, inferior colliculus evoked responses in mutants were small in amplitude and abnormal in waveform. Latencies were long and thresholds were elevated by at least 50 dB at all frequencies tested. These data suggest that the genetic hearing impairment in quivering mice is retrocochlear.

Action Potentials↗
PubMedDate not supplied

Inner ear pathology in the deafness mutant mouse.

A distinctive cochlear pathology was found in deafness mutant mice. There was a delay in the formation of the fluid-filled Nuel and tunnel spaces in the organ of Corti, the hair cells were distorted and degenerate, and there was poor maintenance of synapses. No hair cells appeared normal by TEM, but SEM revealed some areas where stereocilia appeared relatively normal, suggesting that SEM of the surface of the organ of Corti is not necessarily a good indicator of hair cell pathology in hereditary hearing impairment. Mutant mice show normal development of endocochlear potential, but have no measurable cochlear microphonics or compound action potential. The data suggest that the deafness gene affects the organ of Corti and that cochlear hair cells in deafness mice are never functional.

Action Potentials↗
PubMedDate not supplied

Brainstem responses in the quivering mutant mouse.

The recessive quivering gene in mice produces general neurological abnormalities and deafness. Previous work indicated that cochlear responses (microphonics and compound action potentials) were normal in the quivering (qv/qv) mouse, but inferior colliculus evoked potentials had poor thresholds and abnormal latencies. The object of the present study was to record evoked potentials from the cochlear nucleus (CN) in quivering and control mice, and also to record surface responses. The CN evoked response in control mice consisted of two prominent positive peaks. The first peak appeared normal in the quivering CN, resulting in normal thresholds for detection of the response. However, the second peak in mutants was smaller and of longer latency. Surface responses in quivering showed a normal first wave followed by an abnormal wave pattern. It was concluded that the input from auditory nerve to CN in quivering is probably normal and that the central deficit in quivering is evident at the level of CN.

Animals↗