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Biomedical subjects

B Canlon

Publications and source records attributed to B Canlon.

52 records · Page 3Linked to original sources
PubMed1988

The effect of acoustic trauma on the tectorial membrane, stereocilia, and hearing sensitivity: possible mechanisms underlying damage, recovery, and protection.

The aim of the present investigation was to determine: 1) the relationship between changes in auditory sensitivity and alterations in stereocilia micromechanics and tectorial membrane morphology after acoustic overstimulation; 2) the rate of growth of a threshold shift in stereocilia following in vitro overstimulation; and 3) if the damaging effects of noise trauma can be reduced by pre-exposure to a low level acoustic stimulus. After exposure to a 1.0 kHz pure tone signal at 105 dB SPL for 72 hours, the threshold of the auditory brainstem response was broadly elevated by approximately 40-50 dB; the inner hair cell stereocilia became less stiff; and morphological alterations were observed in the middle zone of the tectorial membrane. The location of both the stereocilia and tectorial membrane alterations corresponded to the region of the cochlea demonstrating a threshold shift. Following a recovery period from overstimulation, the auditory brainstem response showed some improvement yet a 25 dB threshold shift remained. At this time, swelling of the afferent dendrites beneath the inner hair cells was observed together with scattered outer hair cell loss. Also, the inner hair cell stereocilia regained their normal stiffness characteristics. The in vitro experiments demonstrated that overstimulation reduced the stiffness of the inner and outer hair cell stereocilia bundles. A threshold shift increased systematically with exposure duration and intensity. After 6 minutes of overstimulation, the threshold shift exhibited a plateau whose magnitude was dependent upon the exposure intensity. Stereocilia micromechanics were shown to be dependent on the metabolism of the hair cell. The pre-treatment to a low level acoustic stimulus (81 dB SPL) prior to exposure to a stimulus known to yield a permanent threshold shift resulted in a 20 dB reduction in the threshold shift relative to the group not pre-exposed as well as complete recovery from the threshold shift after 2 months.

Animals↗
PubMed1987

The postnatal development of stimulated deoxyglucose uptake into the mouse cochlea and the inferior colliculus.

The effect of acoustic stimulation on the postnatal development of deoxyglucose uptake into the mouse cochlea and the inferior colliculus was evaluated. Animals between postnatal day 4 and 20 were separated into four different groups depending on their age. Tritiated deoxyglucose was injected intraperitoneally into each animal and tracer uptake was quantitated by microdissection of the tissues and scintillation counting. Acoustic stimulation at a noise level of 100 dB (A) resulted in supra-normal levels of deoxyglucose uptake for all auditory tissues during postnatal days 13, 14, and 15. The lateral wall tissues, which are non-sensory and non-neuronal, also increased deoxyglucose uptake following acoustic stimulation in a manner that paralleled the uptake by the sensory structures. Serum radioactivity and glucose levels remained unchanged during postnatal development, with these parameters remaining stable with acoustic stimulation.

Acoustic Stimulation↗
PubMed1987

Acoustic overstimulation alters the morphology of the tectorial membrane.

After a permanent threshold shift was induced by exposing guinea pigs to a 1 kHz pure tone at 105 dB(A) for 72 h, light microscopic observations of freshly dissected and stained tectorial membranes showed an increased waviness and clumping of the fibers of the middle zone. Hensen's stripe was not seen as a continuous dense structure running through the middle zone but was at times discontinuous and curved. As measured from cross-sections of the cochlea, the thickness of the tectorial membrane was decreased after acoustic overstimulation. The stereocilia of the inner and outer hair cells lie directly under the middle zone. Visual detection levels of threshold of tectorial membrane movement was determined by stimulating the marginal zone of the tectorial membrane of isolated cochlear coils by an oscillating water jet. After acoustic overstimulation the tectorial membrane became more complaint. The tectorial membrane abnormalities were restricted to the regions of the cochlea that demonstrated a 40-50 dB hearing loss.

Animals↗
PubMed1987

Pure tone overstimulation changes the micromechanical properties of the inner hair cell stereocilia.

The effect of permanent noise-induced hearing loss on the auditory brainstem response (ABR) and the micromechanical properties of cochlear hair cell stereocilia in guinea pigs was investigated. The threshold of movement of the stereocilia was measured by applying force from a fluid filled pipette. After exposure to a 1.0 kHz pure tone signal at 105 dB(A) for 72 h the threshold of the ABR was broadly elevated by approximately 50 dB. Inner hair cell stereocilia showed a decrease in threshold while the outer hair cell stereocilia bundles remained unaltered. This effect was localized to the 13-15 mm distance from the stapes corresponding to the region of maximal stimulation. The effect was recorded within 1 h of exposure and remained constant with exposures up to 7 days. Following a one month recovery period from sound exposure, normal threshold values of stereocilia movement were observed, indicating recovery. At this time, swelling of the afferent dendrites beneath the inner hair cells was observed throughout the cochlea together with approximately 30% scattered loss of outer hair cells in the 13 to 15 mm region. The ABR showed some recovery (approximately 20 dB), yet a threshold shift remained.

Acoustic Stimulation↗
PubMed1986

Changes in stereocilia micromechanics following overstimulation in metabolically blocked hair cells.

Previous studies have demonstrated that stereocilia micromechanics change during exposure to intense stimulation, and then recover after the stimulus has ended. These changes were associated with a loss of stiffness in the sensory hair bundle. The patterns of growth and recovery in these data suggest that active cellular processes control and limit these phenomena. The present investigation further supports this suggestion. The effects of intense stereocilia stimulation were examined before and after the hair cells were metabolically blocked by cooling or by poisoning with NaCN. In normal cells threshold shift increases with exposure duration, reaching a plateau within 5 to 6 min. Moreover, a post-exposure recovery of the threshold was also noted in the control cells within 15 min. In contrast threshold shift after the first minute in the metabolically blocked cells increased monotonically during the exposure without any indication of a plateau. Similarly, no post-exposure recovery of threshold shift was seen in the stereocilia bundles. These data support the hypothesis that metabolic processes in the region of the sensory hairs are important for limiting the loss of stiffness during exposure, as well as for restoring stiffness during recovery.

Animals↗
PubMed1986

Growth of threshold shift in hair-cell stereocilia following overstimulation.

Sensory hair bundle micromechanics were measured from all four hair-cell rows in the isolated guinea pig cochlea before and during overstimulation. The stereocilia bundle was stimulated by an oscillating water jet, and stroboscopic illumination slightly offset from the frequency of the stimulus revealed their motion. The intensity of the water jet could be varied in decibel steps and a 'visual detection level' threshold of stereocilia movement served as the criterion response. Pre-exposure thresholds provided a reference and were compared to thresholds sampled at 1-min intervals during a 10-min exposure period. The exposure stimulus consisted of the water jet adjusted to either 8, 13, or 18 dB above the visual detection level. Stereocilia on hair cells in each of the four rows showed a loss in stiffness which systematically increased during the first 5 to 6 min of exposure. Between 6 and 10 min of overstimulation the threshold shift exhibited a plateau whose magnitude was proportional to the exposure level. There were also differences in the magnitude of threshold shift between the hair-cell rows. The results clearly showed that overstimulation changed the micromechanical behavior of the stereocilia bundle, and that there was a complex interaction between exposure duration, level, and hair-cell row.

Acoustic Stimulation↗
PubMed1984

Glucose utilization in the auditory system: cochlear dysfunctions and species differences.

Deoxyglucose uptake in peripheral auditory tissues and inferior colliculus of the young CBA or C57BL/6J mouse increases with intensity of an acoustic stimulus from 25 to 85 dBA and decreases from 85 to 115 dBA. In 36-month-old CBA and 9-month-old C57BL with sensorineural hearing loss the metabolic response to stimulation is attenuated 50% or more. Metabolic responses to stimuli are qualitatively and quantitatively different in the gerbil and in the guinea-pig. It is concluded that cochlear dysfunctions are characterized by abnormal evoked metabolism; and that the stimulus-response pattern varies with species.

Acoustic Stimulation↗
PubMed1983

Acoustic stimulation alters deoxyglucose uptake in the mouse cochlea and inferior colliculus.

Deoxyglucose uptake and activities of hexokinase and glucose-6-phosphatase in auditory structures (organ of Corti, stria vascularis and spiral ligament, modiolar section of VIIIth nerve, inferior colliculus) and non-auditory tissues (heart, kidney, liver) of the mouse were analyzed. [3H]Deoxyglucose was given as a pulse into the tail vein and uptake was quantitated by microdissection of tissues and scintillation counting. Radioactivity in cochlear tissues was maximal after 45-60 min and declined with a half-life of 30-60 min. Deoxyglucose 6-phosphate represented ca. 60% of total radioactivity (heart, inferior colliculus, greater than 80%). The ratio of hexokinase to glucose-6-phosphatase activity was considerably lower in the auditory periphery than in brain. The rank order was inferior colliculus much greater than VIIIth nerve approximately equal to heart greater than stria vascularis and spiral ligament greater than kidney greater than organ of Corti approximately equal to liver. Exposure to broadband noise increased glucose utilization in all auditory structures. Uptake was maximally (2- to 3-fold) stimulated at moderate noise intensity (55-85 dBA). In addition, the auditory system showed two salient features: at high intensities (100 and 115 dBA) deoxyglucose uptake decreased from the maximum; and the non-sensory tissues of the cochlea (stria vascularis and spiral ligament) responded to sound parallel to the sensory structures at all levels of stimulus intensity. There were no effects of acoustic stimulation on serum glucose levels, serum kinetics of deoxyglucose, or deoxyglucose uptake into other body tissues.

Acoustic Stimulation↗
PubMed1983

Gentamicin ototoxicity dissociated from glucose uptake and utilization.

The hypothesis was tested that gentamicin causes loss of cochlear microphonic potentials by interfering with glucose transport or metabolism in cochlear structures. Gentamicin (3 or 10 mM), applied by perilymphatic perfusion in the guinea pig, reduced cochlear microphonics in a dose-dependent manner. The presence of 5 mM glucose lowered the initial rate but not the final (60 min) loss of cochlear microphonics. Glucosamine (2-deoxy-2-aminoglucose), a reported inhibitor of glucose transport, had no effect at concentrations as high as 20 mM. Glucose utilization was measured by introducing radiolabeled deoxyglucose into the perfusate and determining its uptake into inner ear tissues. Concentrations of deoxyglucose-6-phosphate in organ of Corti and in stria vascularis increased linearly with time and remained unaffected by the presence of 3 mM gentamicin. Ten mM gentamicin reduced deoxyglucose uptake by 30% in the lateral wall tissues but not in the organ of Corti preparation. The lack of correlation between loss of microphonics and glucose utilization does not support interference with glucose metabolism as a primary mechanism of aminoglycoside ototoxicity.

Animals↗
PubMed1981

The effect of noise on deoxyglucose uptake into inner ear tissues of the mouse.

The uptake of deoxyglucose into inner ear tissues was studied in the mouse. Sixty minutes after a single i.v. injection of 5 mCi 2-deoxy-D-[3H]glucose/kg body weight, stria vascularis/spiral ligament and organ of Corti as well as other body tissues were dissected and analyzed for radioactivity. Uptake into inner ear tissues was three to five times lower than into brain or heart. The ratio of deoxyglucose-6-phosphate to deoxyglucose was 60:40 and the compounds were eliminated from the inner ear with a half life of approximately 60 min. Exposure to 100 dB of white noise during the radioactive pulse decreased uptake of deoxyglucose into both stria vascularis/spiral ligament and organ of Corti by 50%.

Animals↗
PubMedDate not supplied

Peripheral cell loss related to calcium binding protein immunocytochemistry in the dorsal cochlear nucleus in CBA/CaJ mice during aging.

The influence of cochlear hair cell and spiral ganglia neuron loss on calcium binding protein immunoreactivity (calretinin, parvalbumin and calbindin) in the dorsal and posteroventral cochlear nuclei (DCN and PVCN) in CBA/CaJ (CBA) mice during aging (1-39 months) was determined. Since calcium binding proteins have buffering properties against calcium overload, they may have a protective role during aging. It is shown that the percentage of calretinin- and parvalbumin-immunopositive neurons in the DCN showed a statistically significant positive correlation with inner hair cell loss, outer hair cell loss, and spiral ganglion cell loss. A correlation was also found between aging and the auditory periphery, and calcium binding proteins in the DCN. These findings imply that the pathophysiological state of the auditory periphery may influence the neuronal homeostasis in the dorsal cochlear nucleus.

Aging↗
PubMedDate not supplied

Succinic dehydrogenase histochemistry as an early marker for hair cell pathology.

Density measurements of succinic dehydrogenase (SDH) activity were obtained from the inner and outer hair cells on surface preparations obtained from the guinea pig cochlea. Guinea pigs were exposed to noise (3.85 kHz, 120 dB SPL, 22.5 min) and sacrificed 0, 4 or 24 h after the exposure. By 4 h after exposure, the first- and second-row outer hair cells already demonstrated an altered SDH activity. By 24 h after exposure, a significant decrease in SDH staining in both the inner and outer hair cells at a distance of 10-12 mm from the cochlear apex was demonstrated. After a 1-month recovery period, scanning electron microscopy confirmed the main lesion site to be at a distance of 10-12 mm. In addition, Hensen's cells (supporting cells) at a distance of 10-12 mm from the apex were intensely stained by SDH after noise exposure, indicating an increase in oxidative metabolism. SDH staining in the Hensen's cells from the unexposed cochleae was not found. In conclusion, our findings suggest that the early use of SDH histochemistry can predict later permanent damage to the organ of Corti.

Animals↗
PubMedDate not supplied

Outer hair cell activity is not required for the generation of the forward masking curve.

Forward masking of the auditory brainstem response (ABR) was achieved by increasing the time interval from 0 to 12 ms between the masker offset and the probe onset. The forward masking response demonstrated a near linear function with an approximate 3.0-dB increase in masking threshold for every millisecond interval increase in the control guinea pig. The slope of the masking curve at selected frequencies together with the quantification of hair cell loss through the analysis of cochlear surface morphology was studied before and after chemical insult. The intracochlear infusion of sodium salicylate caused an approximately 45-dB threshold shift of the ABR whereas the slope of the forward masking curve was not significantly different from the control values at the tested frequencies (1, 4, and 8 kHz). Systemic kanamycin administration (400 mg/kg body weight for 9 consecutive days) caused a permanent ABR threshold shift of 43-63 dB at 1, 4, and 8 kHz. The slope of the forward masking curve was not significantly different at 1 kHz despite significant outer hair cell loss. The slope of the forward masking curve at 4 and 8 kHz showed significant reductions at the time intervals between 0 and 4 ms. Analysis of the kanamycin-treated cochleae revealed not only significant outer hair cell loss throughout the cochlea but significant inner hair cell and inner pillar cell loss in the basal end of the cochlea. The results suggest that the outer hair cells are not needed for maintaining a normal forward masking curve, whereas the slope of the forward masking curve is sensitive to alterations induced to either the inner hair cells or the inner pillar cells.

Animals↗
PubMedDate not supplied

Forward masking is dependent on inner hair cell activity.

The goal of this study was to test the hypothesis that the inner hair cell complex (inner hair cell and dendritic contacts) is solely responsible for generating the slope of the forward masking curve. To test this hypothesis two experiments were performed. The first was to measure forward masking from the Bronx waltzing mouse, a mutant possessing an inner hair cell defect. The Bronx waltzing mouse demonstrated an approximately 60-dB auditory brainstem response (ABR) threshold shift compared to CBA/CBA mice at 8 and 12 kHz. The slope of the forward masking curve was significantly reduced compared to the control group, particularly at the early delay times between 0 and 4 ms. The second model employed kainic acid to affect the dendrites beneath the inner hair cell. After the intracochlear infusion of kainic acid, there was an approximately 47-dB ABR threshold shift at 4 and 8 kHz compared to pre-infusion thresholds. The slope of the forward masking curve from the kainic-acid group was significantly reduced compared to the artificial-perilymph group. Primarily the early delay times were affected by kainic acid (0-4 ms). Morphological analysis showed that there was extensive swelling of the afferent nerve radial dendrites under the inner hair cells. The results from the present study, as well as the preceding article, suggest that the analysis of the slope of the forward masking curve may be used for the detection of inner hair cell or radial dendrite damage, independent of outer hair cell damage. The present finding could provide a useful means of employing a clinical test for determining the function of the inner hair cell complex using a non-invasive measure of auditory function.

Animals↗
PubMedDate not supplied

Differences in forward masking after a temporary and a permanent noise-induced hearing loss.

The forward masking curve of the auditory brainstem response (ABR) at selected frequencies together with the quantification of hair cell loss through the analysis of cochlear surface morphology was studied in guinea pigs before and after acoustic trauma resulting in either a temporary or a permanent threshold shift. In the presence of a noise-induced temporary threshold shift, the slope of the forward masking curve was not significantly different from the pre-exposure curve. In contrast, during the acute phase of the permanent threshold shift, the slope of the forward masking curve was significantly reduced compared to the pre-exposure value. After a recovery period of 2 weeks, the slope of the forward masking curve from the permanently damaged group returned to nearly normal values despite a persisting ABR threshold shift and significant loss of outer hair cells. The potential for analyzing the slope of the forward masking curve in order to distinguish between the acute phase of a permanent threshold shift and a temporary threshold shift is discussed.

Animals↗