Search PubMed⌕ Search

Biomedical subjects

K R Henry

Publications and source records attributed to K R Henry.

At least 73 records · Page 4Linked to original sources
PubMed1982

Age-related changes in sensitivity of the postpubertal ear to acoustic trauma.

Although the age of the postpubertal mammal is typically ignored in evaluating the damaging effects of noise on the ear, it was shown to account for over 65% of the variability in the mouse. 44 inbred CBA/J mice, ranging in age from 60 (early postpuberty) to 360 days (late middle age), were tested for cochlear AP thresholds at frequencies from 2 to 64 kHz. They were then subjected to 5 min of a 124 dB octave band (12-24 kHz) noise. Although all the mice had similar pre-exposure thresholds, the extent of noise-induced AP threshold elevation and the frequencies most severely affected depended upon the ages of the mice. The youngest subjects had the greatest threshold elevations, being most pronounced at, and 1 octave above, the center frequency of the noise exposure. With increasing age there was a progressively less severe effect. The oldest subjects had cochlear AP threshold elevations which were restricted to a frequency 2 octaves above the exposure frequency.

Action Potentials↗
PubMed1982

Age-related auditory loss and genetics: an electrocochleographic comparison of six inbred strains of mice.

A genetic baseline was established for age-related auditory loss in the laboratory mouse (Mus musculus). Auditory nerve isoelectric thresholds were obtained in young, middle aged, and elderly mice at frequencies from 2 to 64 kHz. Six inbred strains of diverse genetic origin and widely varying life spans (298 to 774 days) were examined. Each strain displayed an age-related loss similar to that most often seen in the aging human (i.e., high-frequency losses occurred earliest, followed by losses of middle, and then of lower frequencies). The ranking of these strains in terms of the best to the poorest cochlear function in old age is as follows: SJL/J, AU/SsJ, AKR/J, A/J, C57BR/cdJ, and LP/J. Males and females were equally affected by the aging process.

Acoustic Stimulation↗
PubMed1981

Increased ototoxicity in both young and old mice.

Preweanling, postadolescent, and post-middle-aged CBA/J mice received injections of kanamycin sulfate for two weeks, followed by electrocochleographic (isoelectric auditory nerve-evoked potential thresholds from 2,000 to 64,000 Hz) and histocochleographic (hair cell counts from cochlea whole-mount preparations) analysis. The preweanling mice had structural and functional losses from all portions of the cochlea, while the postadolescent mice had no structural and minimal functional loss. The oldest mice had basal inner and outer hair cell loss and elevated high frequency thresholds. This is an experimental validation of the clinical observation that infants are most susceptible to aminoglycosidic ototoxicity. It also support the suspicion that older persons are also susceptible to ototoxicity and provides the first animal model for experimentally investigating these age-dependent effects.

Aging↗
PubMed1981

Effects of neonatal thyroxine, genotype, and noise on the ear and audiogenic seizures.

Seyfried, Glasser, and Yu recently reported that the DBA/2J mouse genotype, which is innately susceptible to audiogenic seizures, has high neonatal levels of thyroxine (T4) and that neonatal injections of T4 induce susceptibility in the C57BL/6J mouse. In the C57BL/6J mouse, neonatal T4 injections produced a temporary peripheral auditory dysfunction which appeared to be conductive in nature. A cochlear dysfunction was also seen in the DBA/2J mouse and in the acoustically primed C57BL/6J mouse. Since a peripheral auditory threshold elevation in these latter groups of mice appears to be causally related to their susceptibility to audiogenic seizures, it is likely that at least a portion of the susceptibility that Seyfried et al. reported was due to the effects of T4 on the ear.

Acoustic Stimulation↗
PubMed1981

Cholesteatoma: spontaneous occurrence in the Mongolian gerbil Meriones unguiculatis.

Spontaneous aural cholesteatomas were found in thirty-two of seventy ears (45.7 percent) of adult Mongolian gerbils, Meriones unguiculatis. These cholesteatomas arise from the tympanic membrane and the medial ear canal. The advancing front of these cholesteatomas is histologically identical to that of human cholesteatomas. Since the gerbilline cholesteatoma erodes bone and invades the labyrinth and the cranial cavity, it provides an animal model with which to study the destructive properties of human cholesteatoma.

Animals↗
PubMed1980

Age-related auditory loss in the Mongolian gerbil.

Mongolian gerbils were examined for auditory nerve function at five ages, ranging from 90 to 730 days postpartum. Electrocochleograms were obtained in response to tone pips at frequencies ranging from 1 to 64 kHz. An age-related threshold increase was noted at all frequencies. The pattern of auditory loss is different from that observed in the aged rat, guinea pig, and mouse.

Aging↗
PubMed1980

Genotypic differences in behavioral, physiological and anatomical expressions of age-related hearing loss in the laboratory mouse.

The auditory nerve isoelectric thresholds, in response to tone pigs ranging from 5 to 20 kHz, are similar in the young C57BL/6 and CBA/J mice, although the latter genotype has somewhat more sensitive responses from 30 to 80 kHz. But their behavioral audiograms, obtained by the classical conditioning technique of Ehret, are very discrepant. Even though the behavioral audiogram of the CBA/J mouse can be predicted by measurements from its auditory nerve, the behavioral thresholds of the young C57BL/6 mouse are approximately 40 dB less sensitive than its electrophysiological measurements. Cochlear hair cell loss was not evident in young mice of either genotype. As the CBA/J approaches the end of its predicted life span, its auditory anatomy, physiology and behavior are not significantly altered; but those rare individuals, who exceed their predicted life span by 40% finally develop hearing loss of a mixed nature. By contrast, the C57BL/6 mouse shows a relatively rapid decline of hearing as it ages. By 200 days of age, its auditory nerve responses are 30 dB less sensitive at 5 kHz, and 55 dB less sensitive at 30 kHz, than similar measures taken at adolescence. Over this same age span, its behavioral sensitivity has only declined by 15 and 25 dB at these two frequencies. Hair cell counts correlated poorly with both behavioral and electrophysiological auditory measures in the C57BL/6 mouse.

Age Factors↗
PubMed1980

Effects of noise, hypothermia and barbiturate on cochlear electrical activity.

Pentobarbital has been reported as both increasing and decreasing the effects of noise trauma on the inner ear. In the C57BL/6 laboratory mouse, the effects depend upon which electrical events are measured and whether or not the hypothermic effects of pentobarbital are counteracted. Pentobarbital-induced hypothermia per se increased the latency of both the high-intensity-threshold, short-latency (H) and low-intensity-threshold, long-latency (L) waves by approximately 60 mus per degrees C decrease, had no significant effect on H-wave amplitude, but caused a severe reduction of the L-wave amplitude. As little as 1 min of 120 dB SPL high-frequency noise can temporarily reduce the cochlear microphonic (CM) amplitude, abolish the H and reduce the amplitude of the L waves of the click-evoked, volume-conducted gross auditory nerve action potential (AP). 1 week later, CMs were more depressed in subjects which had been anesthetized during 5 min noise exposure, regardless of body temperature during the exposure. The long-term decrement of the L-wave amplitude did not consistently differ as a function of anesthetic state or body temperature at exposure. However, hypothermia protected from, while barbiturate increased the effects of noise stress on the H wave. It was hypothesized that metabolic factors differentially affect the various electrical generators in the inner ear.

Animals↗
PubMed1979

Differential changes of auditory nerve and brain stem short latency evoked potentials in the laboratory mouse.

Subcollicular, volume-conducted auditory evoked potentials were obtained from the C57BL/6 laboratory mouse. Barbiturate-induced, whole body hypothermia was associated with a latency increase; between 37 and 31 degrees C, these values were 0.28, 0.48, 0.88 and 0.88 msec for PI-IV, respectively. The amplitude of the auditory nerve potential elicited by a 100 dB click doubled in amplitude between 16 and 42 days post partum. A progressive latency decrease, from PI to PIV, was observed during this age span. Acoustic stress produced differential changes within peripheral and central amplitude and latency measures, and these parameters were also sensitive to the method used to reduce body movement during the recording session. These changes were consistent with anatomical and physiological data from the auditory brain stem of other mammals.

Acoustic Stimulation↗
PubMed1978

Effects of age and stimulus intensity of the far field auditory brain stem potentials in the laboratory mouse.

The vertex-positive, volume-conducted far field response was used to evaluate age-related changes of the 8th cranial nerve and auditory brainstem in the anesthetized C57BL/L mouse. Responses were obtained from stimuli as low as 10 dB (within the 10-20 kHz bandpass). When latencies were compared between 16- and 35-day-old subjects, the older mice had a P1 component which was .175 msec faster, a P2 which was .505 msec faster, a P3 which was .953 msec faster, and a P4 which was 1.315 msec faster. A retest of the younger mice showed that much of this retrocochlear latency decrease occurred between 16 to 18 days postpartum. The latencies of the younger mice were also less likely to decrease as the stimulus intensity was increased from 30 to 70 dB, and this effect was most pronounced at higher neural levels. These age-related changes bear considerable relationship to the development of susceptibility of audiogenic seizures in the mouse.

Aging↗
PubMed1978

Relation of albinism and drugs to the visual evoked potential of the mouse.

The individual and combined influences of pentobarbital and chlorprothixene on the early components of the cortical visual evoked potential (VEP) were examined in the C57BL/6 mouse. Pentobarbital produced a large increase in latency, and chlorprothixene resulted in a smaller latency increase. When these agents were combined, their effects on the VEP latency were antagonistic. The effects of pentobarbital on VEP amplitude varied as a function of flash intensity, and this barbiturate anesthetic also produced qualitative VEP waveform changes. When the congenic albino (c/c) C57BL/6 was compared with the black (+/+) C57BL/6 mouse; pentobarbital anesthesia produced a decrease of latency with increasing stimulus intensity only in the c/c genotype, whereas VEP amplitudes were similarly affected by pentobarbital in both genotypes.

Albinism↗
PubMed1977

Effects of single albino gene substitutions on the performance of mice in a compound avoidance-discrimination task.

Congenic C57BL/6J mice of the +/+, +/c and c/c genotypes were tested for motoric activity, active avoidance and visual discrimination performance in a variant of the Thompson-Bryant box. The three genotypes were observed to be identical in terms of motor activity, but differed greatly with regard to both avoidance and discrimination performance. On the avoidance portion of the task the c gene appeared to act in an additive fashion, with the +/+ mice being superior to the +/c mice, which were in turn superior to the c/c animals. Visual discrimination performance, however, indicated that the + allele operated in a dominant manner; here c/c mice were found to be inferior in performance when compared to either +/+ or +/c animals while no differences were observed between the two pigmented genotypes. Therefore, under the conditions of the present experiment, the albino gene shows incomplete dominance for active avoidance behavior and recessiveness for visual discrimination performance.

Animals↗
PubMed1976

Roles of anoxia and noise-induced hearing loss in the postictal refractory period for audiogenic seizures in mice.

The present series of experiments demonstrated a postictal refractory period for audiogenic seizures in DBA/2J mice, which was not related to hearing loss but apparently was related to anoxia. Unlike many previous studies, Experiment 1 controlled for the effects of noise exposure upon hearing sensitivity and demonstrated reduced susceptibility to subsequent audiogenic seizures for at least 1 hr after initial clonic-tonic convulsions. The postictal refractory period was shown to result from the occurrence of seizures per se, not from noise exposure alone. Experiment 2 demonstrated deficiencies of sensorimotor functions that accompanied reduced postictal seizure susceptibility. The two phenomena had similar time courses of recovery, which suggested a common mechanism, probably anoxia, associated with the initial convulsions. In support of this view, Experiment 3 showed that recovery from both phenomena was expedited by allowing subjects to breathe increased O2. The role of anoxia in fatal convulsions was suggested by the finding that subjects experiencing clonic-tonic convulsions in a high-O2 environment survived without exception. In contrast, seizures of air-breathing controls were almost always fatal. Taken together, the data indicate that the postictal reduced susceptibility to audiogenic seizures was closely related to metabolic depletion (in particular, anoxia). The pattern of recovery of susceptibility further suggests that the effects of anoxia impair the spread of seizure activity through the central nervous system, although the initiation of seizures is also affected for a short time.

Anesthesia, Inhalation↗
PubMed1975

Acute versus chronic acoustic deprivation: effects on auditory evoked potentials and seizures in mice.

C57BL/6J mice are not typically susceptible to audiogenic seizures, but temporary conductive hearing loss (via earplugging) can induce susceptibility in these subjects. The present study observed that a 40-dB hearing loss, beginning at 17 days postpartum, requires 2 days before it induces susceptibility to audiogenic seizures. When this hearing loss occurred only between 17 and 21 days postpartum, seizures were maximally severe 1-2 days after earplug removal. The peak-to-peak amplitudes of the auditory evoked potential (AEP) were also maximal at this same time. But mice deprived of acoustic input between ages 42-46 days exhibited equally large or even larger AEP amplitudes, while not exhibiting susceptibility to audiogenic seizures. Animals at this older age were shown to be capable of convulsing, in that chronic conductive loss from 17-42 days maintained susceptibility to audiogenic seizures. The acoustic deprivation produced both behavioral (audiogenic seizures) and neural (augmented AEP amplitudes) supersensensitivity to sound, but the former requires a critical period, whereas the latter does not. Some degree of residual hearing loss persisted at all ages for approximately 2 days after removal of the earplugs.

Age Factors↗
PubMed1975

Albinism and auditory function in the laboratory mouse. I. Effects of single-gene substitutions on auditory physiology, audiogenic seizures, and developmental processes.

The effects of single-gene albino (c/c) mutations on auditory behavior and physiology were examined in congenic C57BL/6J mice. At 16 days of age, the c gene was additively associated with both reduced auditory functioning and lower body weight: 16-day-old c/c mice had higher auditory evoked potential (AEP) thresholds than +/c mice, which, in turn, had higher thresholds than +/+ mice; +/c mice were also intermediate with regard to body weight. Since these differences had nearly disappeared by 21 days of age, it was concluded that the c genes worked in an additive fashion to delay development during the period previously (Henry, 1967) found critical for inducing susceptibility to audiogenic seizures. At 16 days of age, albino mice (c/c) displayed susceptibility to audiogenic seizures, but nonalbino genotypes (+/c and +/+) were immune to the convulsive effects of sound. This behavior appeared to be a recessive trait at this age. But 5 days later, the behavioral phenotype exhibited incomplete dominance, with the +/c genotype displaying audiogenic seizures intermediate to those seen in the susceptible c/c and the nonsusceptible +/+ genotypes. These behaviors were compared to the thresholds and peak-to-peak amplitudes of the AEP, as seen in the input-output functions. It is suggested that differential development of the auditory systems in these genotypes is causally related to susceptibility to audiogenic seizures.

Acoustic Stimulation↗
PubMed1975

Albinism and auditory function in the laboratory mouse. II. Effects of acoustic priming and cross-fostering.

Albino (c/c) and nonalbino (+/c and +/+) congenic C57BL/6J mice were examined for the effects of acoustic prestimulation (priming) on audiogenic seizures. While no genotypic-specific effects were noticed 1 day after priming, major effects were observed in separate groups of mice tested 5 days after priming. The c/c mice were most susceptible to audiogenic seizures, and no differences were observed between +/c and +/+ mice. While cross-fostering did not change this relationship, it provided protection from acoustic trauma is considered inconclusive because of the interaction of innate- and priming-induced audiogenic seizures in the +/c and c/c mice.

Age Factors↗