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Results for “Cochlear Nerve”

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At least 991 records · Page 55Linked to original sources

PubMed1978

Endolymphatic and intracellular resting potential in the alligator lizard cochlea.

Endolymphatic potential (EP) and intracellular resting potentials (RPs) in the cochlea of the alligator lizard were measured with micropipets. The EP (defined as the dc electric potential recorded between the endolymph in scala media and the perilymph in scala tympani or scala vestibuli) had a mean value of +16 mV (in 96 ears). The RPs (defined as the dc potentials recorded between the intracellular and perilymphatic spaces) were different in the distal portion of the cochlear nerve (range to -56 mV, mean of -23 mV in 158 cells) from those in the region of the basilar papilla (range to -154 mV, mean of -73 mV in 623 cells). In identified cells in the region of the basilar papilla, the mean values of RPs of hyaline epithelial cells (-113 mV in 7 cells) and supporting cells (-93 mV in 13 cells) were more negative than of hair cells (-73 mV in 5 cells). Differences in measured RPs could reflect differences in the resting potentials of these cells and/or their source resistances. RPs measured in the basilar papilla of the alligator lizard are compared with those obtained in other vertebrate hair cell organs.

Acoustic Stimulation↗

PubMed2000

[Effect of microneurosurgical operation in acoustic neurinoma on symptoms of vertigo and tinnitus].

After exstirpation of an acoustic neuroma one trends to concentrated on the preservation of hearing and facial function. But how does the surgical removal for an acoustic neuroma, influence the symptoms of tinnitus and vertigo? Our report follows a retrospective evaluation of 78 patients. Based on these results we will also discuss aspects of the origin of these symptoms. Our patients suffered from tinnitus at a rate of 73% preoperatively and 59% postoperatively. With increasing tumor size tinnitus occurred less often, therefore we considered the size of the tumor exclusively. Also, an intraoperative dissection of the cochlear nerve often did not result in an improvement of the symptoms. Vertigo was stated prooperatively in 44% of the cases, postoperatively in 22%. Again as with tinnitus, there was an inverse relationship between the size of the tumor and the severity of the symptoms. In conclusion a deafferention-like syndrome has to be considered as the major causative factor for the tinnitus in patients with acoustic neuromas. However, in the vertigo cases, the symptoms seem to be caused vestibularily due to the increasing tumor and then after a temporary compensation a cerebellar ataxia occurred which the patients often perceive as vertigo.

Adolescent↗

PubMed2005

Synaptic influences of pontine nuclei on cochlear nucleus cells.

Using the in vitro isolated whole brain preparation of the guinea pig, we tested the synaptic effects induced by the stimulation of pontine nuclei (PN) in intracellularly recorded and stained principal cells of the cochlear nucleus (CN). Twenty percent of the recorded cells in all CN subdivisions responded to stimulation of either ipsilateral or contralateral PN, and 12% of the cells exhibited convergence of inputs from both sides. The responses were recorded only in stellate cells of the ventral CN and in the pyramidal cells of the dorsal CN, whereas no responses were observed in bushy, octopus, and giant cells. PN stimulation produced excitatory and inhibitory postsynaptic potentials as well as mixed responses. The heterogeneous nature and the wide latency range (3.2-18 ms) of observed responses suggest significant variability in the underlying synaptic mechanisms and the implicated pathways. We propose that PN projections to the CN, terminating mainly in the granule cell domain (GCD), together with other non-auditory and auditory inputs contribute to multimodal convergence in the GCD leading ultimately to modulatory actions on the output activity of CN principal cells.

Animals↗

PubMed2004

Onset neurones in the anteroventral cochlear nucleus project to the dorsal cochlear nucleus.

Considerable circumstantial evidence suggests that cells in the ventral cochlear nucleus, that respond predominantly to the onset of pure tone bursts, have a stellate morphology and project, among other places, to the dorsal cochlear nucleus. The characteristics of such cells make them leading candidates for providing the so-called "wideband inhibitory input" which is an essential part of the processing machinery of the dorsal cochlear nucleus. Here we use juxtacellular labeling with biocytin to demonstrate directly that large stellate cells, with onset responses, terminate profusely in the dorsal cochlear nucleus. They also provide widespread local innervation of the anteroventral cochlear nucleus and a small innervation of the posteroventral cochlear nucleus. In addition, some onset cells project to the contralateral dorsal cochlear nucleus.

Animals↗

PubMed1985

The acute deafness of definite multiple sclerosis: BAEP patterns.

Of 705 patients with or suspected of multiple sclerosis who underwent evoked potential recording during a 5 year period, 12 patients with definite multiple sclerosis experienced an acute hearing loss during a relapse of the demyelinating disease. Hearing loss was unilateral in all of the 12 cases but one; tinnitus was associated with hearing loss in 9 of the 12 patients. Deafness is an unfrequent symptom in the course of multiple sclerosis, being estimated to be no more than 3% in large series of multiple sclerosis. Brain-stem auditory evoked potentials were recorded in all 12 patients, during the relapse with acute hearing loss in 4 of them, after the relapse with hearing loss in the 8 others. During the relapse with hearing loss, BAEP abnormalities were present ipsilateral to the hearing loss in all 4 patients, wave I being absent in 2 of them. BAEPs were drastically improved when recorded after the relapse with hearing loss in 2 of the 3 patients in whom repeated records were made. BAEPs were abnormal on the side of the previous hearing loss in 5 out of the 8 patients recorded after the relapse with hearing loss. Clinical and BAEP data suggest that, in accordance with the anatomical organization of the auditory pathways, the lesion causing unilateral hearing loss in multiple sclerosis could be situated in the cochlear nerve or close to its entry zone in the brain-stem. However, dissociation between unilateral hearing loss and a normal peak I and I-III interval may occur.

Acoustic Stimulation↗

PubMed1993

Effect of a Ca2+ entry blocker, nilvadipine, on hearing disturbances and equilibrium dysfunction caused by microcirculatory disorders of the rat inner ear.

We evaluated the effects of Ca2+ entry blockers, nilvadipine and flunarizine, on microcirculatory disorders of the inner ear and on blood flow in the inner ear of rats. Under sodium pentobarbital anesthesia, the middle ear was opened by a ventrolateral approach. A green light (wave length 540 nm) was applied to the cochlea or the vestibule to induce a hearing disturbance or equilibrium dysfunction as a result of inner ear microcirculatory disorders, while rose bengal solution was infused intravenously. In a hearing disturbance model, a compound cochlear nerve action potential was recorded by electrocochleography every minute after the beginning of illumination. The sound stimulus was an 8 kHz sine wave 100 dB normal hearing level. The action potential was calculated 128 times. The action potential disappeared about 12 min after the beginning of illumination. In another model of equilibrium dysfunction, the photoillumination was applied for 40 min under the infusion of rose bengal. The behavior of rats was observed in the swimming test and nystagmus was recorded 24 h after the completion of photoillumination. In a separate experiment, blood flow in the inner ear was measured with a laser Doppler flowmeter under sodium pentobarbital anesthesia. In this study, both nilvadipine and flunarizine prolonged the time required for complete suppression of the action potential, prevented equilibrium dysfunction in the swimming test and reduced the occurrence of nystagmus. Flunarizine significantly increased inner ear blood flow and nilvadipine failed to decrease blood flow in the inner ear, despite a reduced systemic blood pressure. In conclusion, Ca2+ entry blockers may prevent microcirculatory disorders of the inner ear in rats.

Acoustic Stimulation↗

PubMed1990

Screening procedure for assessment of ototoxicity in the common marmoset.

Detection of drug-induced ototoxicity in safety evaluation studies of novel chemical entities is rarely attempted. Where such examinations are included, they usually rely on reflex testing. The Brainstem Auditory Evoked Response can be measured with the use of externally positioned electrodes, and it monitors electrophysiologic responses to sound from the cochlear nerve and associated structures of the 8th cranial nerve. These responses have been reproducibly measured in sedated marmosets and the method shown to be a sensitive detector of hearing loss caused by loop diuretics or aminoglycoside antibiotics. additionally, where hearing damage is reversible, recovery can also be monitored. It is proposed that where a sensitive marker for ototoxicity is considered necessary as part of a multifaceted study investigating in vivo drug safety, this procedure may prove advantageous over existing methods.

Animals↗

PubMed1988

Cholecalcin (28-kDa CaBP) in the rat cochlea. Development in normal and hypothyroid animals. An immunocytochemical study.

The distribution of cholecalcin (28-kDa calcium-binding protein) in the cochlea of developing rats was followed by immunocytochemistry. In normal animals, the protein first appeared in utero in the cells of Kölliker's organ, a structure involved in the secretion of the tectorial membrane. The inner hair cells, followed by the outer hair cells, then became immunoreactive from the base of the cochlea to the apex. Their cuticular plate, the anchoring structure for stereocilia, was particularly labeled. The cells of Kölliker's organ lost their immunoreactivity after the first postnatal week, the time when they lose their secretory activity. During the same period, when the tunnel of Corti and the space of Nuel open, labeling appeared in the supporting cells. The neurons of the spiral ganglion were stained from the second postnatal week and the fibers of the cochlear nerve after the end of the first month. No difference was induced by thyroid deficiency until the second postnatal week. Thereafter, Kölliker's organ did not transform and its cholecalcin immunoreactivity persisted, together with the secretory activity. As a result, the tectorial membrane was greatly distorted and the mechanical properties of the organ of Corti were dramatically impaired. The supporting cells were labeled although the tunnel of Corti and the space of Nuel did not open. Staining of the spiral ganglion neurons was delayed. All the nervous structures of the cochlea were, however, stained at the end of the first postnatal month, as in normal animals, despite the irreversible complete deafness. Cholecalcin is thus present during development of the cochlea in both non-neuronal and neuronal structures, and is probably involved in very different processes in various types of cells.

Aging↗

PubMed1996

Olivocochlear innervation of inner and outer hair cells during postnatal maturation: an immunocytochemical study.

Changes in the expression of several neurochemical markers associated with either axonal growth (GAP-43), synaptic vesicles (synaptophysin), or the cholinergic population of lateral olivocochlear (OC) efferents were investigated in the postnatal cochlea of hamsters. Growth-associated protein was expressed in the neonatal cochlea but not in the adult; immunoreactivity was found below inner hair cells (IHCs) from postnatal day (P) 2 through P14 and below outer hair cells (OHCs) from P5 to P14. In contrast, synaptophysin was expressed in both the neonate and adult cochlea; immunoreactivity was found below IHCs around P4 and below OHCs at P5. Both GAP-43 and synaptophysin immunoreactivities occurred first below IHCs in basal regions of the cochlea. Efferent fibers containing calcitonin gene-related peptide (CGRP) immunoreactivity were identified as early as P4 within the cochlear nerve but were not observed underneath IHCs until P7. Similar to GAP-43 and synaptophysin immunoreactivity, CGRP expression followed a basal to apical gradient; however, expression below OHCs appeared restricted to apical regions. These data raise the possibility that efferents expressing growth proteins and efferents expressing synaptic vesicle proteins co-exist during the first postnatal week. Furthermore, it is hypothesized that CGRP-containing lateral OC neurons form part of a later, secondary innervation to the cochlea.

Animals↗

PubMed1994

Chronological changes of auditory brainstem responses in Cockayne's syndrome.

Cockayne's syndrome (CS) is a rare autosomal recessive premature-aging disorder which is clinically characterized by physical and mental retardation, retinal pigmentation, sensorineural deafness and other neurological abnormalities. Auditory brainstem responses (ABRs) and behavioral audiometry were studied in 4 cases of confirmed CS chronologically. In one case, ABRs were normal at first but became abnormal. Initially, ABRs revealed only wave I with prolonged latency and thereafter no response. In another case, ABRs revealed the absence of all waves beyond wave III and then revealed the disappearance of all waves. In 2 other cases, ABRs were absent from the first testing. Behavioral levels were elevated in all 4 cases. In 2 cases, behavioral levels did not change in spite of partial disappearance of ABR waves, but they had elevated severely since all waves including wave I disappeared. Our findings suggest that the disease spreads from the upper brainstem to the cochlear nerve and that the site of the lesion causing hearing loss in CS is in the brainstem lesion as well as the peripheral one.

Adolescent↗

PubMed1993

Altered distribution of synaptic densities at aberrant synapses in the chick cochlear nucleus.

The role of axon-target cell interactions in shaping the prevalence and distribution of synaptic densities was studied in an experimentally-induced aberrant functional projection from the chick cochlear nucleus (nuc. magnocellularis, NM) to the contralateral NM. Contact with an abnormal target appears to induce in the aberrant axons a pattern of presynaptic densities resembling that in normal cochlear nerve endings in NM. NM axon terminals induced similar numbers of postsynaptic densities (PSDs) per unit length of membrane apposition in both their normal and abnormal targets but the longer membrane apposition in the highly invaginated aberrant terminal in NM results in a significantly greater amount of postsynaptic density per ending. These auditory neurons thus appear able to adjust a variety of features to permit assembly and maintenance of a novel functional synapse.

Animals↗

PubMed1987

Relationship of serum bilirubin levels and hearing impairment in newborn infants.

A comparison has been made between 39 infants with a birthweight of 1500 g or less and a bilirubinlevel of 240 mumol/l or above, born between January 1980 and December 1983 and 19 infants with the same criteria, born between January 1984 and December 1985. Eight of the 22 high risk and two of the 17 low risk infants were diagnosed to have sensorineural deafness (SND) during the first period and this was strongly associated with the duration of the hyperbilirubinaemia. During the second period, more active intervention for hyperbilirubinaemia led to an increased number of exchange transfusions and a marked drop in the mean duration of hyperbilirubinaemia (less than 240 mumol/l). None of the very low birth weight (VLBW) infants born in the second period have developed SND. To investigate the independent effect of hyperbilirubinaemia on hearing, six low risk infants with bilirubin levels less than 320 mumol/l were studied by serial auditory brainstem responses (ABR). Impairment of the ABRs was found in four infants, with further deterioration with the persistence of high bilirubin levels in two. Although recovery of hearing thresholds was noted in all infants with impaired ABRs, an absence of wave I was noted in three infants at 6 months of age, which could indicate damage to the auditory nerve-cochlear complex. These findings suggest that hyperbilirubinaemia in itself can have an adverse effect on hearing and that careful management of hyperbilirubinaemia may reduce the incidence of sensorineural deafness.

Deafness↗

PubMed1983

Noise-induced degeneration in the brain and representation of inner and outer hair cells.

Noise that destroys receptor cells in the chinchilla cochlea also results in degeneration of axonal endings in the brain from the cochlear nerve fibers and the auditory pathways ascending to the superior olivary complex and inferior colliculus. The patterns of degeneration provide experimental evidence for differential representation of inner and outer hair cells and their functions.

Animals↗

PubMed1987

Incorporation of palmitic acid in the organ of Corti as revealed by autoradiography.

The sites of incorporation of [3H]palmitic acid perfused through the scala tympani of the guinea pig cochlea were localized autoradiographically. The most active incorporation occurred in the lipid globules of Hensen's cells, followed by the hair cells, myelin of the cochlear nerve and other cells. It is speculated that the lipid globules of Hensen's cells act as a reservoir of the vitamin A esterified by fatty acids.

Animals↗

PubMed1991

Postnatal maturation of spiral ganglion neurons: a horseradish peroxidase study.

Using an in vitro cochlear preparation from postnatal hamsters, spiral ganglion cells (SGCs) were labeled retrogradely following extracellular injections of HRP into the cochlear nerve. In 24 cochleae from hamsters between postnatal days (P) 0 and 10, the neuronal morphology of 201 SGCs and their peripheral axons were analyzed. From P 0 to 3, labeled SGCs had few distinguishable features. Although SGCs could be traced separately to inner hair cells (IHCs) and outer hair cells (OHCs), they all had roughly bipolar-shaped cell bodies. Approximately half of the labeled SGCs had peripheral axons that spiraled some distance before entering radial fiber bundles. From P 3 to 7, SGCs increased in size by nearly 30% and the number of SGCs with spiraling peripheral axons decreased to near zero. At P 10, the central axon diameter to peripheral axon diameter ratios distinguished two populations of SGCs. The hair-cell innervation patterns of SGCs also changed morphologically as a function of postnatal age. At P 0, radial fiber (RF) terminals of peripheral axons contacted as many as 8 IHCs; by P 3, RFs contacted typically one or two IHCs. The terminal portions of peripheral axons contacting OHCs did not show any appreciable spiral until P 2. By P 5, individual outer spiral fibers (OSFs) had greater spiral lengths underneath row-3 OHCs and the number of OHC contacts was also greatest for row-3 OSFs. These data suggest that SGCs undergo a systematic maturational process. Furthermore, the morphological differentiation of SGCs occurs after they have established separate inner and outer hair cell innervations.

Age Factors↗

PubMed2005

Regulation of the timing of MNTB neurons by short-term and long-term modulation of potassium channels.

The firing patterns of neurons in central auditory pathways encode specific features of sound stimuli, such as frequency, intensity and localization in space. The generation of the appropriate pattern depends, to a major extent, on the properties of the voltage-dependent potassium channels in these neurons. The mammalian auditory pathways that compute the direction of a sound source are located in the brainstem and include the connection from bushy cells in the anteroventral cochlear nucleus (AVCN) to the principal neurons of the medial nucleus of the trapezoid body (MNTB). To preserve the fidelity of timing of action potentials that is required for sound localization, these neurons express several types of potassium channels, including the Kv3 and Kv1 families of voltage-dependent channels and the Slick and Slack sodium-dependent channels. These channels determine the pattern of action potentials and the amount of neurotransmitter released during repeated stimulation. The amplitude of currents carried by one of these channels, the Kv3.1b channel, is regulated in the short term by protein phosphorylation, and in the long term, by changes in gene expression, such that the intrinsic excitability of the neurons is constantly being regulated by the ambient auditory environment.

Action Potentials↗

PubMed2005

The effect of dorsal cochlear nucleus ablation on tinnitus in rats.

A growing body of evidence implies that the dorsal cochlear nucleus (DCN) plays an important role in tinnitus. To test the hypothesis that the rostral output of the DCN is necessary for the experience of chronic tinnitus, the dorsal DCN and the dorsal acoustic stria of rats with psychophysical evidence of tinnitus was ablated. If the DCN plays a necessary role in the generation of chronic tinnitus, ablating the DCN should decrease the evidence of tinnitus in subjects previously shown to have tinnitus. Contrary to prediction, bilateral dorsal DCN ablation did not significantly (n=11, p=0.707) affect the psychophysical evidence of tinnitus, and ipsilateral dorsal DCN ablation appeared to increase the evidence of tinnitus (n=9, p=0.018) compared to pre-ablation performance. It was concluded that the DCN does not act as a simple feed-forward source of chronic tinnitus. Alternative hypotheses were considered, among them that elevated DCN activity following acoustic trauma triggers persistent pathological changes distributed across more than one level of the auditory system. In addition to serving as a trigger, the DCN may also modify the experience of tinnitus, since the evidence of tinnitus was enhanced by ipsilateral DCN ablation.

Acoustic Stimulation↗

PubMed2005

Tinnitus as a plastic phenomenon and its possible neural underpinnings in the dorsal cochlear nucleus.

Tinnitus displays many features suggestive of plastic changes in the nervous system. These can be categorized based on the types of manipulations that induce them. We have categorized the various forms of plasticity that characterize tinnitus and searched for their neural underpinnings in the dorsal cochlear nucleus (DCN). This structure has been implicated as a possible site for the generation of tinnitus-producing signals owing to its tendency to become hyperactive following exposure to tinnitus inducing agents such as intense sound and cisplatin. In this paper, we review the many forms of plasticity that have been uncovered in anatomical, physiological and neurochemical studies of the DCN. Some of these plastic changes have been observed as consequences of peripheral injury or as fluctuations in the behavior and chemical activities of DCN neurons, while others can be induced by stimulation of auditory or even non-auditory structures. We show that many parallels can be drawn between the various forms of plasticity displayed by tinnitus and the various forms of neural plasticity which have been defined in the DCN. These parallels lend further support to the hypothesis that the DCN is an important site for the generation and modulation of tinnitus-producing signals.

Cochlear Nerve↗