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Cochlear sensitivity in the lesser spear-nosed bat, Phyllostomus discolor.

Behavioral auditory thresholds of Phyllostomus discolor are characterized by two threshold minima separated by an insensitive region at about 55 kHz (Esser and Daucher 1996). To investigate whether these characteristics are due to cochlear properties, we recorded distortion product otoacoustic emissions (DPOAEs) and calculated relative DPOAE threshold curves, which proved to be a good measure of cochlear sensitivity. Our results indicate that in P. discolor, cochlear sensitivity, as assessed by DPOAE recordings, does not show a threshold maximum at 55 kHz. The DPOAE threshold curves display an absolute minimum at approximately 30 kHz, and from that frequency region, the threshold continuously increases without any pronounced irregularities. The frequency tuning properties of the cochlea, as assessed by DPOAE suppression tuning curves (STCs) reveal broad filter bandwidths with Q10dB values between 3.4 and 10.7. There are no frequency-specific specializations of cochlear tuning. The characteristic pattern of subsequent threshold maxima and minima at high frequencies observed in behavioral studies seems to be shaped by transfer characteristics of the outer ear and/or neuronal processing in the ascending auditory pathway rather than by cochlear mechanics.

Animals↗

Localization of neurotensin immunoreactivity in neurons and organ of Corti of rat cochlea.

The distribution of neurotensin-containing cell bodies and fibers has been observed in the central and peripheral nervous system, including sensory ganglia, but no description has been found in the peripheral auditory system. Here, we investigated the presence of neurotensin immunoreactivity in the cochlea of the adult Wistar rat. Strong neurotensin immunoreactivity was detected in the cytoplasm of the inner hair cells (IHC) and Deiters' cells of the organ of Corti. Outer hair cells (OHC) show weak immunoreaction. Neurotensin immunoreactivity was also found in the neurons and fibers of the spiral ganglia. Quantitative microdensitometric image analysis of the neurotensin immunoreactivity showed a strong immunoreaction in the hair cells of organ of Corti and a moderate to strong labeling in the spiral ganglion neurons. A series of double immunolabeling experiments demonstrated a strong neurotensin immunoreactivity in the parvalbumin immunoreactive IHC and also in the calbindin immunoreactive Deiters' cells. Weak neurotensin immunoreactivity was seen in the calbindin positive OHC. Neurofilament and parvalbumin immunoreactive neurons and fibers in the spiral ganglia showed neurotensin immunoreactivity. Calbindin immunoreactivity was not detected in the spiral ganglion neurons, which are labeled by neurotensin immunoreactivity. The presence of neurotensin in the cochlea may be related to its modulation of neurotransmission in the peripheral auditory pathway.

Animals↗

Recording of electrical-evoked responses from a remote field in the vestibular part of the eighth nerve. A preliminary technical report.

The paper discusses the results of the author's own studies concerning the recording of electrical responses evoked from a remote field in the vestibular part of the eighth nerve. The studies are of experimental nature and they were carried out repetitively in guinea pigs. Particular attention is paid to an apparatus specially designed and constructed, permitting to obtain stimulation of adequate quality of vestibular organs, and to receive and average short (up to 10 ms) evoked vestibular potentials. Different variants of elimination of bioelectrical muscular disturbances and of the auditory pathway are proposed.

Acceleration↗

[Study on the bilaterally recorded ABR in the experimental model of acoustic tumor].

The ABRs were bilaterally recorded with monaural stimulation from the animal model of acoustic tumor in 10 rats. It was found that the waveform of ABRs recorded from the right dura was different from the left one. A major feature of right ABRs was that the amplitudes of wave II and wave III were decreased by 3.53 +/- 1.21 microV and 3.94 +/- 1.16 microV respectively, and that the latencies of wave IV and wave V were increased by 0.88 +/- 0.11ms and 1.37 +/- 0.10ms respectively. It suggested that the cochlear nerve near the cochlear nucleus was pressured. A major feature of left ABRs was that the amplitudes of wave III were prominently reduced by 7.02 +/- 0.73 microV and wave IV and V were mixed together. The results implied that the waves generated after wave III might be affected by the bilateral auditory pathway.

Acoustic Stimulation↗

Projections of physiologically characterized spherical bushy cell axons from the cochlear nucleus of the cat: evidence for delay lines to the medial superior olive.

Bushy cells in the anteroventral cochlear nucleus (AVCN) receive their principal excitatory input from the auditory nerve and are the primary source of excitatory input to more centrally located brainstem auditory nuclei. Despite this pivotal position in the auditory pathway, details of the basic physiological information being carried by axons of these cells and their projections to more central auditory nuclei have not been fully explored. In an attempt to clarify these details, we have physiologically characterized and anatomically labeled individual axons of the spherical bushy cell (SBC) class of the cat AVCN. The characteristic frequencies (CFs) of our injected SBC population are low, all less than 12 kHz and primarily (83%) less than 3 kHz, while their spontaneous activity is comparatively high (mean of 59 spikes/sec). In response to short tone bursts at CF, low CF (< 1 kHz) SBC units can phase-lock better than auditory nerve fibers. SBCs with CFs above 1 kHz have primary-like responses at all stimulus levels and can show robust phase-locking to an off-CF, 500 Hz tone. When compared with our previously reported population of labeled globular bushy cells (GBC; Smith et al., 1991, J. Comp. Neurol. 304:387-407), some similarities and differences are apparent in both physiological response properties and axonal projection pattern. GBCs show no low frequency bias in CFs, have lower spontaneous rates, and the high CF units exhibit a primary-like-with-notch response at high stimulus levels as a consequence of a very well timed onset component. Low CF, GBC short tone responses are indistinguishable from those of SBCs. Anatomically, the axons of SBCs cross the midline in the dorsal component of the trapezoid body and typically innervate the medial superior olive (MSO) on both sides, the ipsilateral lateral superior olive (LSO), and the contralateral ventral nucleus of the lateral lemniscus (VNLL). The projections to the contralateral, but not the ipsilateral MSO, show a rostral to caudal delay line configuration, similar to the scheme first proposed by Jeffress (1948, J. Comp. Psychol. 41:35-39). The form of this delay line is consistent with the topographic map of interaural time delays reported by Yin and Chan (1990, J. Neurophysiol. 64:465-488). Projections to the ipsilateral LSO often take an indirect route. In contrast, GBC axons travel in the ventral component of the trapezoid body, never innervate the MSO, rarely innervate the ipsilateral LSO, and always innervate the contralateral medial nucleus of the trapezoid body. The terminal specializations of both SBC and GBC axons contain round vesicles.

Animals↗

Electrical stimulation of the cochlear nerve in deafness mice.

The deafness mouse mutant provides a useful animal model for studying the central consequences of complete auditory deprivation during development. The object of this study was to record inferior colliculus-evoked potentials in mutant and control mice, using short electrical pulses to stimulate either the whole cochlea or the cochlear nerve directly. In both experiments, evoked potentials were readily recorded in the mutant and control mice, indicating that some central connections are functional, even though the auditory pathway has received no stimulus-related input throughout development. The results are relevant to the clinical problem of restoring auditory function in the profoundly deaf using peripheral electrical stimulation.

Animals↗

Brainstem auditory evoked response at five years and prenatal and postnatal blood lead.

Previous work from this laboratory demonstrated an association between higher maternal blood lead level at 20 weeks of pregnancy and increased I-V and III-V interpeak intervals in the brainstem auditory evoked response (BAER) recorded in 1-month-old infants. We repeated the BAER measurements with a larger group of children (n = 100-113) from the same study at 5-7 years. Maternal blood lead level at 20 weeks of pregnancy (geometric mean = 7.7 microg/dl; range 1-30. 5 microg/dl) was the only prenatal blood lead level significantly associated with I-V and III-V interpeak interval in a multiple regression model controlling for head circumference and age at time of testing and sex. In contrast to the findings at 1 month of age, interpeak intervals decreased as a linear function of increasing 20-week maternal blood lead. A nonlinear, orthogonal, second-order polynomial model was a significantly better fit to the data than the linear model. The nonlinear model showed I-V and III-V interpeak intervals decreased as blood lead rose from 1 to 8 microg/dl, and then increased as blood lead rose from 8 to 30.5 microg/dl. We hypothesized that the negative linear term was related to lead effect on brainstem auditory pathway length, and that the positive quadratic term was related to neurotoxic lead effect on synaptic transmission or conduction velocity. We found support for the brainstem length interpretation in the data, showing that 6-year-old head circumference in these children significantly decreased with increased maternal 20-week blood lead level. Increasing postnatal blood lead at 12 and 48 months was related only to decreased BAER conduction intervals across the entire blood lead range, suggesting only pathway length effects. Alterations in BAER at this age may indicate that the effect of prenatal lead exposure on the auditory brainstem is permanent, as response latencies reach essentially adult values by 4 years of age.

Analysis of Variance↗

Evolution of GABAergic circuitry in the mammalian medial geniculate body.

Many features in the mammalian sensory thalamus, such as the types of neurons, their connections, or their neurotransmitters, are conserved in evolution. We found a wide range in the proportion of gamma-aminobutyric acidergic (GABAergic) neurons in the medial geniculate body, from <1% (bat and rat) to 25% or more (cat and monkey). In the bat, some medial geniculate body subdivisions have no GABAergic cells. Species-specific variation also occurs in the somesthetic ventrobasal complex. In contrast, the lateral geniculate body of the visual system has about the same proportion of GABAergic cells in many species. In the central auditory pathway, only the medial geniculate body shows this arrangement; the relative number of GABAergic cells in the inferior colliculus and auditory cortex is similar in each species. The range in the proportion of GABAergic neurons suggests that there are comparative differences in the neural circuitry for thalamic inhibition. We conclude that the number of GABAergic neurons in thalamic sensory nuclei may have evolved independently or divergently in phylogeny. Perhaps these adaptations reflect neurobehavioral requirements for more complex, less stereotyped processing, as in speech-like communication.

Animals↗

A genetic screen for mutations that disrupt an auditory response in Drosophila melanogaster.

Hearing is one of the last sensory modalities to be subjected to genetic analysis in Drosophila melanogaster. We describe a behavioral assay for auditory function involving courtship among groups of males triggered by the pulse component of the courtship song. In a mutagenesis screen for mutations that disrupt the auditory response, we have recovered 15 mutations that either reduce or abolish this response. Mutant audiograms indicate that seven mutants reduced the amplitude of the response at all intensities. Another seven abolished the response altogether. The other mutant, 5L3, responded only at high sound intensities, indicating that the threshold was shifted in this mutant. Six mutants were characterized in greater detail. 5L3 had a general courtship defect; courtship of females by 5L3 males also was affected strongly. 5P1 males courted females normally but had reduced success at copulation. 5P1 and 5N18 showed a significant decrement in olfactory response, indicating that the defects in these mutations are not specific to the auditory pathway. Two other mutants, 5M8 and 5N30, produced amotile sperm although in 5N30 this phenotype was genetically separable from the auditory phenotype. Finally, a new adult circling behavior phenotype, the pirouette phenotype, associated with massive neurodegeneration in the brain, was discovered in two mutants, 5G10 and 5N18. This study provides the basis for a genetic and molecular dissection of auditory mechanosensation and auditory behavior.

Animals↗

Auditory and visual evoked potentials to irrelevant stimuli during conditioning to a visual stimulus.

Amplitude changes of evoked responses to irrelevant auditory (click) and visual (optic tract stimulation) stimuli were examined during appetitive conditioning to a flashing light. Four female cats, with chronically implanted electrodes along the visual and auditory pathways, were conditioned with pairings of a flashing light and food reinforcement. The results showed that, as conditioning progressed, the auditory evoked potentials were attenuated while the visual evoked potentials did not change significantly. The data seem to indicate possible differences in the neural processing of irrelevant information.

Animals↗

Auditory neuropathy.

Ten patients presented as children or young adults with hearing impairments that, by behavioural and physiological testing, were compatible with a disorder of the auditory portion of the VIII cranial nerve. Evidence of normal cochlear outer hair cell function was provided by preservation of otoacoustic emissions and cochlear microphonics in all of the patients. Auditory brainstem potentials showed evidence of abnormal auditory pathway function beginning with the VIII nerve: the potentials were absent in nine patients and severely distorted in one patient. Auditory brainstem reflexes (middle ear muscles; crossed suppression of otoacoustic emissions) were absent in all of the tested patients. Behavioural audiometric testing showed a mild to moderate elevation of pure tone threshold in nine patients. The extent of the hearing loss, if due to cochlear receptor damage, should not have resulted in the loss of auditory brainstem potentials. The shape of the pure tone loss varied, being predominantly low frequency in five patients, flat across all frequencies in three patients and predominantly high frequency in two patients. Speech intelligibility was tested in eight patients, and in six was affected out of proportion to what would have been expected if the pure tone loss were of cochlear origin. The patients were otherwise neurologically normal when the hearing impairment was first manifest. Subsequently, eight of these patients developed evidence for a peripheral neuropathy. The neuropathy was hereditary in three and sporadic in five. We suggest that this type of hearing impairment is due to a disorder of auditory nerve function and may have, as one of its causes, a neuropathy of the auditory nerve, occurring either in isolation or as part of a generalized neuropathic process.

Adolescent↗

Pathogenesis of hearing loss in head injury. Studies in man and experimental animals.

This study reports on the histopathologic findings in the temporal bones and brain of a patient who died of head injury. A common type of head injury in man was simulated in guinea pigs by shaking them. A hearing loss was demonstrated with Preyer reflex audiometry although the cochlear potential thresholds remained normal. Only minor pathologic changes were found in the membranous labyrinths. Laceration and hemorrhage in and around the cerebrum, rhombencephalon, and eighth nerves were noted in most of the experimental animals. Auditory manifestations following head injury may very frequently be due to damage to the central auditory pathways rather than to the end organ.

Animals↗

Maturation of auditory evoked potentials in young guinea pigs with binaural conductive hearing loss.

A reversible conductive hearing loss produced during the first 4 weeks post partum caused marked alterations in the development of click-evoked auditory brainstem (ABR) and middle latency (MLR) responses in guinea pigs. The early component PI in the ABR in controls showed adult-like latencies at the time of birth, while the later ABR components PIII and PV and all components investigated in the MLR showed postnatal development characterized by a shortened latency that persisted for the whole period of investigation. The course of the ABR latencies showed the sharpest decrease during the first 2-3 weeks of life, while that for the MLR took place during the first 5 weeks. In addition to the increased ABR thresholds and lengthened ABR latencies due to the conductive hearing loss, development of the ABR inter-peak latencies (IPL) and MLR latencies was retarded. The IPL reached control values 1 week after the end of the deprivation phase, while the delay in MLR started later (4th week) and lasted longer than did that in the ABR. These findings showed that a long-lasting postnatal conductive hearing loss does not generate sustained impairment at the level of the brainstem but can evoke longer-lasting deficiencies at higher stations of the auditory pathway.

Aging↗

Modulation of auditory responsiveness in the locust.

The auditory responsiveness of a number of neurones in the meso- and metathoracic ganglia of the locust, Locusta migratoria, was found to change systematically during concomitant wind stimulation. Changes in responsiveness were of three kinds: a suppression of the response to low frequency sound (5 kHz), but an unchanged or increased response to high frequency (12 kHz) sound; an increased response to all sound; a decrease in the excitatory, and an increase in the inhibitory, components of a response to sound. Suppression of the response to low frequency sound was mediated by wind, rather than by the flight motor. Wind stimulation caused an increase in membrane conductance and concomitant depolarization in recorded neurones. Wind stimulation potentiated the spike response to a given depolarizing current, and the spike response to a high frequency sound, by about the same amount. The strongest wind-related input to interneuron 714 was via the metathoracic N6, which carries the axons of auditory receptors from the ear. The EPSP evoked in central neurones by electrical stimulation of metathoracic N6 was suppressed by wind stimulation, and by low frequency (5 kHz), but not high frequency (10 kHz), sound. This suppression disappeared when N6 was cut distally to the stimulating electrodes. Responses to low frequency (5 kHz), rather than high frequency (12 kHz), sounds could be suppressed by a second low frequency tone with an intensity above 50-55 dB SPL for a 5 kHz suppressing tone. Suppression of the electrically-evoked EPSP in neurone 714 was greatest at those sound frequencies represented maximally in the spectrum of the locust's wingbeat. It is concluded that the acoustic components of a wind stimulus are able to mediate both inhibition and excitation in the auditory pathway. By suppressing the responses to low frequency sounds, wind stimulation would effectively shift the frequency-response characteristics of central auditory neurones during flight.

Animals↗

Transdermal nicotine administration enhances automatic auditory processing reflected by mismatch negativity.

Mismatch negativity (MMN) is a component of event-related potentials (ERPs) with a wide-ranging applicability to the investigation of neuronal substrates of information processing in normal and psychopathological states. Nicotine has been shown to be implicated in the pathophysiology of psychiatric disorders as schizophrenia or Alzheimer's disease, and has also been proposed as a self-administered drug in schizophrenia. The goal of the present study is to elucidate the effect of nicotine on the auditory automatic processing reflected by MMN. Nicotine was administered transdermally under controlled dosage. Ten healthy volunteers attended the laboratory for one baseline session and two test sessions. The test sessions involved administration of a placebo patch and a nicotine skin patch, which were counter-balanced. The ERPs were recorded passively during an auditory oddball paradigm. Nicotine administration shortened the MMN latencies, and these effects were independent of the earlier ERP components, N100 and P200. In conclusion, nicotine enhances preattentive and automatic processing such as MMN system and these effects appear to be quite specific and independent of earlier cognitive stages than preattentive mismatch processing. The shortened MMN latency may be interpreted as a reduction of the amount of time required to complete a neuronal mismatch process through the ascending auditory pathway.

Acoustic Stimulation↗

Auditory brainstem response findings in Rett syndrome: stability over time.

OBJECTIVE: To determine whether changes consistent with the presence of white matter neurodegenerative disease would be observed in the auditory brainstem response (ABR) in Rett syndrome in conjunction with age advancement. STUDY DESIGN: Initial and follow-up ABR findings were analyzed in a sample of 27 female patients with Rett syndrome. The interval between ABR tests ranged from 1 to 9 years. RESULTS: No significant group differences consistent with neurodegenerative disease were observed in the wave I-III, III-V, or I-V interpeak latency intervals between the initial and follow-up test sessions. CONCLUSIONS: Rett syndrome is not a disorder characterized by progressive white matter degeneration affecting the integrity of the brainstem central auditory pathways.

Adolescent↗

Brainstem bilirubin toxicity in the newborn primate may be promoted and reversed by modulating PCO2.

The auditory brainstem response (ABR) was monitored during infusion of bilirubin in six ventilated newborn rhesus monkeys (138-145 d gestation) while acute changes in pH were produced by varying inspired CO2. Prolonged respiratory acidosis without bilirubin infusion produced minimal changes in the ABR (one animal). CO2 exposure, usually initiated when the bilirubin level reached approximately 20 mg/dL, decreased arterial pH to values ranging from 6.85 to 7.10. ABR changes, including prolongation of the wave II-IV peak to peak intervals and decreased wave amplitudes, first developed 2-4 h after initial exposure to CO2. Total and unbound bilirubin levels at this time ranged from 376 to 564 mumol/L (22-33 mg/dL) and 38 to 65 nmol/L (2.5-3.8 micrograms/dL), respectively. Correction of respiratory acidosis produced partial to complete reversal of ABR changes within 3 to 20 min. Reexposure to CO2 immediately reproduced the ABR abnormality. Production and reversal of the abnormal ABR was obtained through two to three cycles in three animals. Thus, when the brainstem bilirubin level was near the threshold for toxicity, the effect of changes in PCO2 on the ABR were immediate, suggesting that auditory pathway toxicity is initially mediated by a reversible pH-dependent bilirubin-membrane complex. In contrast to humans, in monkeys auditory toxicity appeared to be a late manifestation of bilirubin toxicity, inasmuch as all monkeys were obtunded and apneic 30-70 min before ABR abnormalities appeared. Notwithstanding these limitations, the results support the hypothesis that bilirubin toxicity can be both promoted and reversed by modulating brain pH.

Acidosis, Respiratory↗

Auditory deficits and hearing loss associated with focal brainstem haemorrhage.

Four cases of central pontine haemorrhage are described in which auditory dysfunction was documented. Two cases had a hearing loss, in one of which there was recovery of the low frequencies. This case provides support for the tonotopic organization of the auditory pathways in the caudal pontine area, with the lowest frequencies being encoded medially. In all cases, there were abnormalities of the auditory brainstem responses, wave V being consistently involved, while wave III was abnormal in only one patient. In three cases, the masking level differences and crossed acoustic reflex thresholds were abnormal. The ipsilateral reflex thresholds were normal at least on one side in all cases. In the patient with the most significant hearing loss, loudness recruitment, assessed both psychophysically and with the acoustic reflex thresholds, was evident. These data are interpreted in terms of there being damage to the medial superior olivary nuclei and trapezoid body involving both afferent and efferent fibres.

Adult↗