Search PubMed⌕ Search

Biomedical subjects

K R Henry

Publications and source records attributed to K R Henry.

At least 55 records · Page 3Linked to original sources
PubMed1986

Offset tuning curves generated by simultaneous masking are more finely tuned than those generated by forward masking.

The rapid ending of a tone produces an evoked potential which has different properties than that which is produced by the sudden onset of a tone. At the level of the round window, the offset N1 N2 follows the ending of the cochlear microphonic (CM) by approximately the same amount of time as does the onset N1 N2 to the onset of the CM. Both onset and offset responses are abolished with cochlear lesion. Continuous masking was used to generate tuning curves (TCs) from the NI-PI component of the evoked potential recorded from the round window of the gerbil. Those evoked potentials generated in response to the tone onset were complementary in appearance to those generated in response to the tone offset. TCs generated by continuous masking of the NI-PII component of the auditory brainstem response (ABR) of the gerbil show the same pattern. When it is generated by simultaneous masking, the midfrequency offset TC in the gerbil and mouse is W-shaped. It has two well tuned tips which occur at frequencies below and above that of the probe stimulus used to generate the TC. It also has an even better tuned peak occurring at or slightly above the probe stimulus frequency, which becomes sharper as the masker sound pressure level (SPL) is increased from 50 to over 80 dB. Because the midfrequency onset response is approximately 40 dB lower than the midfrequency offset response, probe stimuli for onset TCs are generally set at lower SPLs. When the onset probe stimulus is set to the same level as that of the offset probe, the Q10 dB of the offset TC may be up to 10 times the value of the Q10 dB of the onset TC. The offset TC generated in the CBA/J mouse by forward masking is quite different from that produced by simultaneous masking. Both forward and simultaneous conditions utilized a 40 ms duration tone to mask the PI-NI component of offset and onset ABRs of the mouse which were evoked by a 10 ms duration, 32 kHz tone, presented at an interstimulus interval of 160 ms. Forward masking (when compared with simultaneous masking) resulted in a more sharply tuned onset TC. But the offset TC was much less sharply tuned in the forward masking condition. This suggests that the offset response may reflect functions which are involved with fine tuning at moderate to high intensities in the presence of simultaneous sounds of similar spectral characteristics.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Effects of dietary restriction on presbyacusis in the mouse.

If dietary restriction can extend the human life span, it would be useful to know whether presbyacusis would continue its normal pace. This question was experimentally addressed, using the mouse as a model. Alternate-day feeding and fasting resulted in restricted mice of the AKR and AU/Ss inbred strains weighing less than their continuously fed controls. Restriction did not increase the life span or alter presbyacusis of the AKR mouse, but it improved both functions in the AU/Ss mouse. Their life spans were increased by 40%, and cochlear functions were better than controls at every age at which animals of both groups were still alive. Nonetheless, the oldest remaining restricted AU/Ss mouse had greater cochlear loss than was seen in any AU/Ss control mice. This study demonstrates that dietary restriction can slow the cochlear losses in a mammal which has a presbyacusis condition similar to that of humans.

Animals↗
PubMed1986

Auditory physiology and behavior in RB/1bg, RB/3bg, and their F1 hybrid mice (Mus musculus): influence of genetics, age, and acoustic variables on audiogenic seizure thresholds and cochlear functions.

In the early 1950s, Frings and Frings began a process of selection for audiogenic seizure susceptibility and resistance in albino mice. The present study was conducted to examine behavioral and cochlear functions in the inbred descendants of these mice. The cochlear action potential (AP) thresholds of the susceptible RB/1bg inbred mice were abnormally high, and the resistant inbred RB/3bg mice had normal AP audiograms. The F1 hybrid showed heterosis for its cochlear function. Only the RB/1bg was susceptible to audiogenic seizures on the first acoustic exposure. Thresholds for the successive components of their audiogenic seizures were determined in response to narrow bands of noise. These paralleled the AP thresholds of RB/1bg mice (r = .89). This RB/1bg mouse showed little age-related cochlear loss, which probably accounts for its robust sensitivity to audiogenic seizures over most of its lifespan. Earlier studies had demonstrated that the susceptible RB line had a robust AP, but little or no cochlear microphonic (CM). The susceptible RB/1bg had well-defined AP and CM responses at low frequencies. The nonsusceptible RB/3bg mice were more resistant to acoustic priming than another mouse (CBA/J) strain with a similar audiometric profile.

Acoustic Stimulation↗
PubMed1985

Cochlear function and audiogenic seizures: developmental covariance in the LP/J mouse.

Innate susceptibility to audiogenic seizures develops and declines at varying rates and ages, depending upon genotype and environmental conditions. Auditory dysfunctions have been experimentally produced which induce susceptibility in otherwise nonsusceptible mouse strains. In order to more closely correlate cochlear functions and audiogenic seizures in genetically susceptible mice, both measures were obtained from LP/J mice, at ages ranging from 8 to 120 days. Susceptibility to sound-produced convulsions was first noted at 12 days, was maximal from 18 to 32 days, declined rapidly by 40 days, and disappeared by 120 days of age. Cochlear nerve-evoked potential thresholds were very high at 12 days, were lowest between 18 and 32 days and increased thereafter. The correlation between susceptibility and cochlear thresholds was greatest for high frequencies (r = -.93), intermediate for midfrequency (r = -.77), and poorest for low frequencies (r = -.56). It was concluded that either genetic or environmental factors which produce an intermediate level of high frequency cochlear damage in the young mouse will produce susceptibility to audiogenic seizures.

Acoustic Stimulation↗
PubMed1985

ON and OFF components of the auditory brainstem response have different frequency- and intensity-specific properties.

When the ear of the mouse is stimulated with a tone burst of sufficiently long duration, a stimulus offset evoked potential is generated which mirrors, in some respects, the onset auditory brainstem response (ABR). The general waveform and interpeak latencies suggest this offset response is generated within the cochlea and auditory brainstem. But when visual detection threshold audiograms are made for these two responses, their shapes are not similar. The onset ABR thresholds reflect the behavioral detection thresholds, being lowest at midfrequency, while the offset thresholds are highest at midfrequency in the normal hearing CBA/J and RB3/bg mice. The LP/J mouse, with a mixed (conductive and sensory) dysfunction, shows a different relationship between its onset and offset thresholds. The onset- and offset-ABRs of the normal mouse also differ from each other in the slopes of their amplitude input-output functions.

Animals↗
PubMed1985

Tuning of the auditory brainstem OFF responses is complementary to tuning of the auditory brainstem ON response.

Continuous masking studies show a complementary pattern of effects on the auditory brainstem responses (ABRs) which are generated by the onset and by the offset of a midfrequency tone. The masking profiles of the two responses are almost opposite with a probe stimulus frequency of 32 kHz (16-32 kHz is the midfrequency region for the CBA/J mouse). The Offset and Onset ABR tuning curves (TCs) also reveal very different properties at the midfrequencies of 16, 20, 24 and 32 kHz. The Offset TC is exquisitely sensitive to masking by very low intensity stimuli at a narrow range of frequencies which are lower than the probe stimulus frequency. Continuous masking produces a well-tuned low frequency tip to the Offset TC. For Offset TCs generated in response to midfrequency tones, the Q+10 dB of this tip averages 8.3. Masking at this low frequency tip of the Offset TC has no observable effect on the Onset ABR. The Offset ABR is also sensitive to masking by a narrow range of frequencies which are higher than the probe stimulus frequency. This occurs at an intensity which also has no observable effect on the Onset ABR. The Q+10 dB of this high frequency tip averages 9.2. The average frequencies where these Offset TC tips occur fit the cubic difference formula (2f1-f2), which describes a distortion product of two-tone suppression. At low probe stimulus frequencies, there is only a high frequency Offset TC tip; at high stimulus frequencies, only a low frequency tip. The high frequency tip has a higher threshold and appears more susceptible to metabolic disturbance. The Offset ABR TC also has a peak which corresponds to the probe stimulus frequency. Continuous masking with the stimulus frequency produces nonmonotonic enhancement of the Offset ABR, while it simultaneously reduces the magnitude of the Onset ABR. The tuning of this Offset TC peak (measured as Q-10 dB) is almost always much sharper than the corresponding Onset TC tip in the same mouse. These values for midfrequency stimuli average 6.2 for the Onset, and 13.6 for the Offset TCs. This fine tuning of the Offset TC at the probe stimulus frequency occurs at SPLs from 50 to more than 90 dB.

Animals↗
PubMed1985

Extra-high-frequency noise remotely masks and alters temporal integration at lower frequencies.

A quasi-free-field technique was used to assess the effects of extra-high-frequency-band masking on detection threshold of middle and high (1-7 kHz) frequencies. At an SPL of 60 dB, the 10- to 20-kHz masker produced a slight amount of masking. Increasing the masking level by another 5 dB produced a disproportionate increase of the detection thresholds. This increase was greatest in response to 4- and 5-kHz stimuli, and was detected with both constant and pulsed tones. Decreasing the bandwidth of the masker reduced the magnitude of the effect, but not the frequency-specific pattern of the remote masking. Extra-high-frequency masking also increased the amount of temporal integration at middle and high frequencies. The data are discussed in reference to peripheral and central neural changes associated with sensorineural hearing loss.

Adult↗
PubMed1985

Extra-high-frequency auditory thresholds: fine structure, reliability, temporal integration and relation to ear canal resonance.

Three trained subjects were repeatedly tested for detection of auditory thresholds at 27 frequencies, from 2 to 18 kHz. A double-blind procedure was used with the method of adjustment, and the quasi-free-field delivery system of Osterhammel et al. [Scand. Audiol. 6:91-95, 1977] was used to monaurally stimulate the ear. A very reliable series of high- and low-threshold changes, termed the fine structure of the extra-high-frequency audiogram, was observed from 8 to 16 kHz. All 6 ears had a major low-threshold region at or near 13.5 kHz, and up to 3 other replicable sensitive frequencies along this one octave range. Thresholds were invariant over 3 conditions of stimulus presentation (constant tone; 500 ms duration, 25 ms rise and decay, 1 s interstimulus interval; and 100 ms duration, 1.5 ms rise and decay, 200 ms interstimulus interval). As the duration of the tone was decreased from 100 to 5 ms, temporal integration (an average of approximately 2.5 dB threshold increase as the duration was halved) was noted. Although temporal integration was slightly less at higher frequencies, the shape of the audiograms remained essentially unchanged as the stimulus duration was decreased to 5 ms. There was no consistent relationship between the maximally sensitive high frequencies and the amount of temporal integration. But there was a general association between the maximally sensitive high frequencies and the resonant frequency characteristics of that particular ear.

Adult↗
PubMed1984

Cochlear microphonics and action potentials mature and decline at different rates in the normal and pathologic mouse cochlea.

A technique is described that can nontraumatically assess cochlear microphonic (CM) and cochlear action potential (AP) thresholds to pure tones in the intact mouse. This method was applied to the normal hearing CBA/J, and to the C57BL/6J, which has early-onset hearing loss. CM thresholds are most sensitive in both mice by 23 days of age, and the C57BL/6J CM responses degenerate rapidly thereafter, especially at the high-frequency end. The CMs of the CBA/J continue to change past 23 days, developing a threshold dip at 24 kHz, and becoming slightly less sensitive at 32 kHz. The AP of the C57BL/6J is also most sensitive at 23 days, and becomes gradually less sensitive to 32- and 64-kHz tones over the next 36 days. The CBA/J AP thresholds are not maximally sensitive until 41 days of age.

Age Factors↗
PubMed1984

Hypothermia protects the cochlea from noise damage.

Thresholds of the cochlear action potential were obtained from rodents at euthermic (38 degrees C) and hypothermic (30 degrees and 25 degrees C) rectal temperatures. In the gerbil, low and middle frequency (1-8 kHz) thresholds increased an average of 2.3 dB per degrees C decrease of body temperature; at 16 kHz, 3.5 dB/degrees C; and at 32 kHz, an increase of 4.4 dB/degrees C. In the mouse, these values were: 2-16 kHz, 1.4 dB increase per degrees C decrease; 32 kHz, 2.7 dB/degrees C; 64 kHz, 3.8 dB/degrees C. When subjects maximally susceptible to permanent threshold shift (PTS) at low and middle frequencies (anesthetized, immature mice) were exposed to 115 dB noise, hypothermia reduced PTS at these most susceptible frequencies (2-16 kHz). When awake adult mice were exposed to this noise, hypothermia protected them from PTS at their most vulnerable frequency (32 kHz).

Animals↗
PubMed1984

Cochlear damage resulting from exposure to four different octave bands of noise at three ages.

Three age-groups of CBA/J inbred mice were exposed for 5 min to one of four octave bands of 124-dB noise. The ages corresponded to weaning (20 days), early postpuberty (60 days), and adulthood (180 days). Threshold shifts of the electrocochleographically obtained cochlear nerve action potential were determined 4 days following the noise exposure. Pure-tone bursts of 2-64 kHz were used to elicit these responses. Noise-induced threshold shifts (NITS) were progressively greater in those responses that originated from a more basal (high-frequency) portion of the organ of Corti. The 3--6-kHz noise band did not affect thresholds; 6--12- and 12--24-kHz bands produced a NITS of 25--30 dB; and 24--48-kHz noise produced a NITS of at least 18 dB. The 20- and 60-day-old subjects were more severely affected (25 and 23.5 dB average NITS, respectively) than the 180-day-old mice (9.5 dB NITS). Susceptibility to damage at the apex and middle of the organ of Corti declined as a function of age during exposure. But the base of the organ of Corti remained equally susceptible to damage from 6-12-, 12-24-, or 24-48-kHz noise bands, from weaning age to adulthood. When these data were compared with those from another study, it was concluded that an early sensitive period exists for noise-induced damage to the apex and middle of the organ of Corti but that the base maintains its susceptibility for a much longer age span.

Age Factors↗
PubMed1984

Noise and the young mouse: genotype modifies the sensitive period for effects on cochlear physiology and audiogenic seizures.

A sharply defined "critical period" has been described for the young C57BL/6 mouse, during which acoustic trauma will profoundly alter subsequent auditory behavior (audiogenic seizures, acoustic startle reflex). In several genotypes and species, a broader "sensitive period" exists, during which acoustic trauma is most damaging to cochlear functions in the young ear. In order to examine the correspondence of these two events, C57BL/6 and CBA inbred mice, at eight ages ranging from 12 to 54 days, were exposed to 2 min of a 124-dB (SPL) octave band noise (8-16 kHz). A noninvasive electrocochleographic technique was used to assess cochlear microphonic (CM) and action potential (AP) thresholds in exposed mice and their nonexposed littermate controls. This allowed cochlear functional measures and behavioral tests (susceptibility to audiogenic seizures) to be made in the same animals. Noise has no observable effect on the 12-day-old CBA mouse, produced a maximal threshold elevation (47 dB for AP, 28 dB for CM) at 30-36 days, with the effect declining to nearly half of this value in 54-day-old subjects. Susceptibility to audiogenic seizures in the exposed CBA mice was greatest at the peak of this sensitive period for cochlear damage (r = .95). C57BL/6 mice also appeared unaffected when noise exposure occurred at 12 days of age; they had maximal AP (23 dB) and CM (17 dB) threshold elevations at 36 days, and 54-day-old mice had an 18-dB elevation of the AP and their CM was no longer affected. Susceptibility to audiogenic seizures was greatest in C57BL/6 mice exposed to noise at 18 days, and it did not correspond with the sensitive period for cochlear damage (r = .21). Therefore, both genotypes have a sensitive period for the effects of noise trauma on the CM and AP, the CBA has a sensitive period for acoustic priming for audiogenic seizures, and the C57BL/6 has a critical period for acoustic priming. Genetic differences in age-related losses of central nervous system auditory functions are postulated as being responsible for these behavioral differences. These data are compared with known auditory functions of the SJL and BALB/c mouse strains in order to explain genetically determined differences of the sensitive (or critical) period of acoustic priming, and for the length of time the mice subsequently remain susceptible to audiogenic seizures.

Acoustic Stimulation↗
PubMed1984

Ultrahigh-frequency auditory thresholds in young adults: reliable responses up to 24 kHz with a quasi-free-field technique.

A quasi-free-field technique was used to assess detection thresholds to pure tones, at frequencies ranging from 2 to 24 kHz. The sound delivery system of Osterhammel et al. [Scand. Audiol. 6:91-95, 1977] was modified in order to deliver constant stimuli at SPLs of at least 117 dB over the entire frequency range. A modified form of the method of adjustment maintained the subjects' interest, and a double-blind procedure minimized experimenter and subject bias. In the first experiment, 78 university subjects from Northern California (18-24 years old) were exposed to tones in 2-kHz increments. All but 12 of these persons could reliably detect the highest frequency, with females being slightly more sensitive. But from 10 to 20 kHz, there were no differences between the sexes. In a second group of 20 students, tested in 1-kHz increments from 8 to 16 kHz, the previously observed 10- to 14-kHz threshold plateau was revealed as a pronounced 13-kHz low-threshold region. The threshold at this frequency was approximately 14 dB lower than the 11-kHz threshold. These data were compared with those obtained in a similar fashion from other cultures.

Adolescent↗
PubMed1983

Otosclerotic lesions in the inbred LP/J mouse.

Inbred LP/J mice develop abnormal bony lesions that are grossly and histologically similar to the lesions of human otosclerosis. This is the first known occurrence of spontaneous otosclerosis-like lesions in an animal. As in the human disease, these lesions impair audition by immobilizing the ossicles of the middle ear. The LP/J mouse may be an animal model for this common human disease.

Animals↗
PubMed1983

Age-related increase of spontaneous aural cholesteatoma in the Mongolian gerbil.

The Mongolian gerbil is the only non-human animal known to spontaneously develop aural cholesteatomas. In this rodent, both the prevalence of spontaneous cholesteatomas and the resultant peripheral auditory evoked potential threshold increases from 6 to 18 months of age. By 24 months, the end of their median life span, other factors begin to affect auditory function. Therefore, the electrocochleographic technique can be efficiently used to nontraumatically trace the development of the cholesteatoma from 6 to 18 months, providing an experimental method for evaluating techniques to prevent or retard the growth of aural cholesteatomas.

Aging↗
PubMed1983

Lifelong susceptibility to acoustic trauma: changing patterns of cochlear damage over the life span of the mouse.

Age-related differences in susceptibility to noise-induced threshold shift (NITS) were examined over the entire life span of the CBA/J mouse. Mice of varying ages were given a single 5-min exposure to a 124-dB octave-band (12-24 kHz) noise. Susceptibility began at 15-16 days postpartum and increased rapidly until approximately 20 days of age. During this phase, NITS (as measured by increased action potential threshold) was greatest at 16 kHz. Overall susceptibility was consistently high from 20 to 90 days. During this phase, NITS became most severe at 32 kHz. From 120 days until beyond the end of its actuarial life span (527 days), NITS no longer occurred at 2-16 kHz, but the 64-kHz response retained its susceptibility to acoustic trauma. Mice at 20 and 60 days of age showed the same pattern of decreasing susceptibility as the intensity of the noise exposure was reduced to 114 and 104 dB, indicating that the absence of a tightly restricted critical period is not peculiar to a particular sound pressure level.

Age Factors↗
PubMed1983

Disparity in the cytocochleogram and the electrocochleogram in aging LP/J and A/J inbred mice.

The auditory systems of aging LP/J and A/J inbred mice were studied using electrocochleography (AP thresholds) and surface preparation cytocochleography. Both strains showed marked age-related auditory threshold elevation, the LP/J demonstrating more pronounced elevation with age than the A/J. Surprisingly, the cytocochleograms showed the opposite relationship: the A/J strain had more loss of hair cells than the LP/J. The elevation of AP thresholds of the LP/J mouse was far out of proportion to the expected auditory deficit on the basis of the cytocochleogram alone. Auditory deficits in the aging LP/J mouse must be due to factors other than anatomical loss of sensory cells.

Aging↗