Aging and the auditory brainstem response in mice with severe or minimal presbycusis

doi:10.1016/0378-5955(87)90137-7

Hearing Research

Volume 30, Issues 2–3, 1987, Pages 207-218

https://doi.org/10.1016/0378-5955(87)90137-7 Get rights and content

Abstract

Threshold, latency, and amplitude of the auditory brainstem response (ABR) were obtained with filtered noise pips in young and aging C57BL/6J mice (to 16-months), which undergo severe progressive age-related sensorineural hearing loss (presbycusis) and CBA/J mice (to 19-months), which show only mild loss late in life. Aging per se (CBA mice) is not associated with significant changes in ABR parameters. Presbycusis, in aging C57 mice, is associated with increased thresholds; there is a trend toward increased latencies, but only when threshold elevations are substantial. Amplitudes of early waves, but not late waves, decrease greatly in aging C57 mice. In young C57 mice, amplitudes of early ABR waves vary monotonically with intensity, while amplitudes of later waves (IV and V) have a relatively flat, or even nonmonotonic, relationship to intensity; in older C57 mice, all waves have monotonie intensity functions. ABR parameters are not affected by gender in either strain. The mouse models can help to clarify some inconsistencies in the human literature on aging and the ABR.

References (34)

T. Allison et al.
Brain stem auditor, pattern-reversal visual, and short-latency somatosensory evoked potentials: Latencies in relation to age. sex. and brain and body size. Electroencephalogr
Clin. Neurophysiol.
(1983)
T. Allison et al.
Developmental and aging changes in somatosensory, auditory and visual evoked potentials
Electroencephalogr. Clin. Neurophysiol.
(1984)
N. Chu
Age-related latency changes in the brain-stem auditory evoked potentials
Electroencephalogr. Clin. Neurophysiol.
(1985)
J. Harrison et al.
Auditory brainstem responses in the aged cat
Neurobiol. Aging
(1982)
U. Rosenhall et al.
Brain-stem auditory evoked potentials in different age groups
Electroencephalogr. Clin. Neurophysiol.
(1985)
M.J. Rowe
Normal variability of the brain-stem auditory evoked response in young and old adult subjects
Electroencephalogr. Clin. Neurophysiol.
(1978)
G.V. Simpson et al.
Altered peripheral and brainstem auditory function in aged rats
Brain Res.
(1985)
J.F. Willott et al.
Excitability of auditory neurons in the dorsal and ventral cochlear nuclei of DBA/2 and C57BL/6 mice
Exp. Neurol.
(1984)
H.A. Beagley et al.
Differences in brainstem response latency with age and sex
Br. J. Audiol.
(1978)
M. Bergman
Hearing in the Mabaans
Arch. Otolaryngol.
(1966)

M. Bergman et al.

Age-related decrement in hearing for speech

J. Gerontol.

(1976)

C.P. Goetzinger et al.

A study of hearing in advanced age

Arch. Otolaryngol.

(1961)

C.S. Hallpike

The loudness recruitment phenomenon: A clinical contribution to the neurology of hearing

C.C. Hansen et al.

Pathological studies in presbycusis

Arch. Otolaryngol.

(1965)

F. Harbert et al.

Audiologic findings in presbycusis

J. Aud. Res.

(1966)

S.W. Harkins

Effects of age and interstimulus interval on the brainstem auditory evoked potential

Int. J. Neurosci.

(1981)

K.R. Henry

Auditory brainstem volume-conducted responses: Origins in the laboratory mouse

J. Am. Audiol. Soc.

(1979)

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Aging and the auditory brainstem response in mice with severe or minimal presbycusis

Abstract

Clin. Neurophysiol.

Electroencephalogr. Clin. Neurophysiol.

Electroencephalogr. Clin. Neurophysiol.

Neurobiol. Aging

Electroencephalogr. Clin. Neurophysiol.

Electroencephalogr. Clin. Neurophysiol.

Brain Res.

Exp. Neurol.

Differences in brainstem response latency with age and sex

Br. J. Audiol.

Hearing in the Mabaans

Arch. Otolaryngol.

Age-related decrement in hearing for speech

J. Gerontol.

A study of hearing in advanced age

Arch. Otolaryngol.

The loudness recruitment phenomenon: A clinical contribution to the neurology of hearing

Pathological studies in presbycusis

Arch. Otolaryngol.

Audiologic findings in presbycusis

J. Aud. Res.

Effects of age and interstimulus interval on the brainstem auditory evoked potential

Int. J. Neurosci.

Auditory brainstem volume-conducted responses: Origins in the laboratory mouse

J. Am. Audiol. Soc.