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At least 595 records · Page 33Linked to original sources
PubMed2003

The zinc finger transcription factor Gfi1, implicated in lymphomagenesis, is required for inner ear hair cell differentiation and survival.

Gfi1 was first identified as causing interleukin 2-independent growth in T cells and lymphomagenesis in mice. Much work has shown that Gfi1 and Gfi1b, a second mouse homolog, play pivotal roles in blood cell lineage differentiation. However, neither Gfi1 nor Gfi1b has been implicated in nervous system development, even though their invertebrate homologues, senseless in Drosophila and pag-3 in C. elegans are expressed and required in the nervous system. We show that Gfi1 mRNA is expressed in many areas that give rise to neuronal cells during embryonic development in mouse, and that Gfi1 protein has a more restricted expression pattern. By E12.5 Gfi1 mRNA is expressed in both the CNS and PNS as well as in many sensory epithelia including the developing inner ear epithelia. At later developmental stages, Gfi1 expression in the ear is refined to the hair cells and neurons throughout the inner ear. Gfi1 protein is expressed in a more restricted pattern in specialized sensory cells of the PNS, including the eye, presumptive Merkel cells, the lung and hair cells of the inner ear. Gfi1 mutant mice display behavioral defects that are consistent with inner ear anomalies, as they are ataxic, circle, display head tilting behavior and do not respond to noise. They have a unique inner ear phenotype in that the vestibular and cochlear hair cells are differentially affected. Although Gfi1-deficient mice initially specify inner ear hair cells, these hair cells are disorganized in both the vestibule and cochlea. The outer hair cells of the cochlea are improperly innervated and express neuronal markers that are not normally expressed in these cells. Furthermore, Gfi1 mutant mice lose all cochlear hair cells just prior to and soon after birth through apoptosis. Finally, by five months of age there is also a dramatic reduction in the number of cochlear neurons. Hence, Gfi1 is expressed in the developing nervous system, is required for inner ear hair cell differentiation, and its loss causes programmed cell death.

Animals↗
PubMed2006

The influence of Er. YAG laser application in fenestration to the inner ear.

OBJECTIVE: Erbium (Er.) YAG laser may be usable for middle ear surgery because of its ability to ablate bony tissue. We investigated the inner ear damage caused by the fenestration to the inner ear with Er. YAG laser. DESIGN: We investigated the influence of Er. YAG laser on the inner ear using electrophysiological technique. RESULTS: Several cases had a decrease in endocochlear potential (EP) and cochlear microphonics (CM) after the fenestration to the inner ear. CONCLUSIONS: Er. YAG laser is safe if it is used for the small and superficial fenestration to the stapes footplate. However, a few extra pulses after fenestration are dangerous.

Acoustic Stimulation↗
PubMed2005

Prospective study of inner ear radiation dose and hearing loss in head-and-neck cancer patients.

PURPOSE: To determine the relationship between the radiation dose to the inner ear and long-term hearing loss. METHODS AND MATERIALS: Eligible patients included those receiving curative radiotherapy (RT) for head-and-neck cancer. After enrollment, patients underwent three-dimensional conformal RT planning and delivery (180-200 cGy/fraction) appropriate for their disease site and stage. The inner ear was contoured on axial CT planning images. Dose-volume histograms, as well as the mean and maximal dose for each structure, were calculated. Patients underwent pure tone audiometry at baseline (before treatment) and 1, 6, 12, 24, and 36 months after RT. The threshold level (the greater the value, the more hearing loss) in decibels was recorded for 250, 500, 1000, 2000, 4000, and 8000 Hz. For patients receiving predominantly unilateral RT, the contralateral ear served as the de facto control. The differences in threshold level between the ipsilateral and contralateral ears were calculated, and the temporal pattern and dose-response relation of hearing loss were analyzed using statistical methods that take into account the correlation between two ears in the same subject and repeated, sequential measurements of each subject. RESULTS: Of the 40 patients enrolled in this study, 35 qualified for analysis. Four patients who received concurrent chemotherapy and RT were analyzed separately. The 31 unilaterally treated patients received a median dose of 47.4 Gy (range, 14.1-68.8 Gy) to the ipsilateral inner ear and 4.2 Gy (range, 0.5-31.3 Gy) to the contralateral inner ear. Hearing loss was associated with the radiation dose received by the inner ear (loss of 210dB was observed in ears receiving >/=45 Gy) and was most appreciable in the higher frequencies (>/=2000 Hz). For a 60-year-old patient with no previous hearing loss in either ear, after receiving 45 Gy, the ipsilateral ear, according to our clinical model, would have a 19.3-dB (95% confidence interval [CI], 15.5-23.0) and 5.4-dB (95% CI, 3.5-7.5) hearing decrement compared with the contralateral ear for 8000 Hz and 1000 Hz, respectively. Age and an initial hearing difference within an ear pair also affected hearing loss. The baseline hearing threshold was inversely related to radiation-induced hearing loss. The degree of hearing loss was dependent on the frequency tested, age, baseline hearing, and baseline difference in hearing between a patient's two ears. CONCLUSION: High-frequency (>/=2000 Hz) hearing acuity worsens significantly after RT in a dose-dependent fashion. A larger number of patients needs to be studied to validate these results. This knowledge can be applied to create guidelines regarding future dose limits to the auditory apparatus for patients undergoing head-and-neck RT.

Age Factors↗
PubMedDate not supplied

Diving injuries to the inner ear.

Most of the previous literature concerning otologic problems in compressed gas environments has emphasized middle ear barotrauma. With recent increases in commercial, military, and sport diving to deeper depths, inner ear disturbances during these exposures have been noted more frequently. Studies of inner ear physiology and pathology during diving indicate that the causes and treatment of these problems differ depending upon the phase and type of diving. Humans exposed to simulated depths of up to 305 meters without barotrauma or decompression sickness develop transient, conductive hearing losses with no audiometric evidence of cochlear dysfunction. Transient vertigo and nystagmus during diving have been noted with caloric stimulation, resulting from the unequal entry of cold water into the external auditory canals, and with asymmetric middle ear pressure equilibration during ascent and descent (alternobaric vertigo). Equilibrium disturbances noted with nitrogen narcosis, oxygen toxicity, hypercarbia, or hypoxia appear primarily related to the effects of these conditions upon the central nervous system and not to specific vestibular end-organ dysfunction. Compression of humans in helium-oxygen at depths greater than 152.4 meters results in transient symptoms of tremor, dizziness, and nausea plus decrements in postural equilibrium and psychomotor performance, the high pressure nervous syndrome. Vestibular function studies during these conditions indicate that these problems are due to central dysfunction and not to vestibular end-organ dysfunction. Persistent inner ear injuries have been noted during several phases of diving: 1) Such injuries during compression (inner ear barotrauma) have been related to round window ruptures occurring with straining, or a Valsalva's maneuver during inadequate middle ear pressure equilibration. Divers who develop cochlear and/or vestibular symptoms during shallow diving in which decompression sickness is unlikely or during compression in deeper diving, should be placed on bed rest with head elevation and avoidance of maneuvers which result in increased cerebrospinal fluid and intralabyrinthine pressure. With no improvement in symptoms after 48 hours, exploratory tympanotomy and repair of a possible labyrinthine window fistula should be considered. Recompression therapy is contraindicated in these cases...

Action Potentials↗
PubMed1998

Effect of lipo-pro-prostaglandin E1, AS-013 on rat inner ear microcirculatory thrombosis.

We investigated effects of lipo-pro-prostaglandin E1 (lipo-[11alpha, 13E, 15S]-11,15-dihydroxy-9-[1-oxobutoxy]-prosta-8, 13-dien-1-oic acid butyl ester), AS-013 in two models of hearing disturbance and equilibrium dysfunction induced by rat inner ear microcirculatory thrombosis. Inner ear microcirculatory thrombosis was induced by photochemical reaction between systemic injection of Rose Bengal and irradiation of green light to the cochlea and vestibule. Photochemical reaction causes endothelial injury followed by platelet adhesion, aggregation and formation of a platelet- and fibrin-rich thrombus. In the hearing disturbance model, a compound cochlear nerve action potential was recorded by electrocochleography every minute. Photochemical reaction induced inner ear microcirculatory thrombosis, followed by disappearance of the action potential. AS-013 significantly (P<0.05) prolonged time to disappearance of the action potential compared with control group. In the equilibrium dysfunction model, the irradiation to the vestibule was applied for 10 min after Rose Bengal injection. The behavior of rats in the swimming test and nystagmus were observed 24 h after the completion of irradiation. In the swimming test, two of 12 animals treated with AS-013 showed no rotating about their longitudinal axes, which indicates equilibrium dysfunction and the duration of well-balanced swimming prolonged. AS-013 suppressed the appearance of nystagmus. These results suggest that lipo-pro-prostaglandin E1, AS-013 may prevent hearing disturbance and equilibrium dysfunction due to inner ear microcirculatory disorders.

Action Potentials↗
PubMed2006

[Orientation of three lysosomal enzymes in the mouse inner ear and hearing loss in enzyme gene deficiency].

OBJECTIVE: To determine the distribution and influence of lysosomal neuraminidase (Neul), protective protein/cathepsin A (PPCA) and beta-galactosidase (beta-gal) in the inner ear of the mouse, and to observe their auditory alterations in enzyme deficiency. METHODS: Six wild type (2 months postnatal) (Neu1+/+, PPCA+/+ and beta-gal+/+) mice were used, and Neu1, PPCA and beta-gal homozygous (Neu1-/-, PPCA-/- and beta-gal-/-) mice at the same age used as control in this experiment. The auditory thresholds were examined through the auditory brainstem responses (ABR) to click, which tone pips were 8, 16, and 32 kHz. The mice were intracardically perfused with 4% paraformaldehyde. The bulla were further fixed in 4% paraformaldehyde, processed and sectioned with paraffin embedded method. Immunohistochemistry was used to determine the cellular localizations of Neu1, PP-CA, and beta gal in the inner ear. RESULTS: There was a similar distributive pattern of Neu1, PPCA and betagal in the inner ear. Neu1 intense staining was observed in the cochlear spiral ganglion cells, spiral limbus, spiral ligament, vestibular ganglion cells, cristae, maculae hair cells, and weak staining in inner hair cells, outer hair cells, supplying cells of the organ of Corti and stria vascularis. The intense staining of PPCA and beta-gal were observed in the spiral ganglion and vestibular ganglion cells, and weak staining in the spiral limbus, spiral ligament, stria vascularis and organ of Corti. The inner ear exhibited no staining when Neul, PPCA and beta-gal were deficient, respectively. A positive staining of PPCA and beta-gal was presented in Neu1-/- mice, and as well as Neu1 and PPCA in beta-gal-/- mice. However, the staining of Neu1 was not presented, and only very weak staining of beta-gal in PPCA-/- mice. The auditory thresholds of Neul, PPCA, and beta-gal mice were elevated for 60-69 dB, 40-48 dB, and 7-10 dB above those of wildtype littermates, respectively. CONCLUSION: Neu1 PPCA and beta-gal are distributed in the inner ear of mouse, and the three enzymes also form a lysosomal multi-enzyme complex in the inner ear. The respective enzyme deficiencies can induce the hearing the loss of different levels.

Animals↗
PubMed2000

Disruption of mdr1a p-glycoprotein gene results in dysfunction of blood-inner ear barrier in mice.

P-glycoprotein (p-gp), a drug transporter in multidrug-resistant cancer cells, is a transmembrane protein encoded by mdr1a, mdr1b and mdr2 genes in mice. In our previous report, high level p-gp was immunohistochemically detected in capillary endothelial cells of the guinea pig inner ear, supporting a possible role as an extrusion pump in the blood-inner ear barrier (BIB). We investigated the functional involvement of p-gp in the inner ear using mdr1a gene knock-out mice [mdr1a(-/-) mice]. Pharmacokinetic analyses showed that mdr1a(-/-) mice displayed obviously increased accumulations of the p-gp-transported drugs doxorubicin (adriamycin, ADM) and vinblastine in the inner ear tissues compared with those in mdr1a(+/+) mice. Subsequent functional studies using auditory-evoked brainstem responses showed hearing impairment only in mdr1a(-/-) mice after administering these drugs. Furthermore, inhibition of p-gp function by co-administration of cyclosporin A (CsA) with doxorubicin (ADM) in mdr1a(+/+) mice resulted in increased accumulation of ADM in inner ear tissues and hearing impairment similar to that noted in mdr1a(-/-) mice. We conclude that mdr1a p-gp, which acts as an efflux pump in the inner ear, prevents ototoxicity induced by p-gp substrate drugs and contributes to a new functional mechanism in the BIB.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

[Inner ear depression after middle ear interventions].

BACKGROUND: Any type of otosurgical procedure involves the risk of inner ear damage. As middle ear surgery is also performed for functional reasons this risk should be taken into consideration. The aim of this study was to analyse the frequency and the nature of sensorineural hearing loss following chronic ear surgery. PATIENTS: A total of 3989 middle ear cases operated on between 1991 and February 1999 at the Department of Otorhinolaryngology, Head and Neck Surgery, University of Würzburg, Germany were studied retrospectively: 781 type I tympanoplasties, 2408 type III tympanoplasties and 800 cases of stapes surgery. The pre- and the postoperative audiograms in the frequency range between 500 and 8000 Hz were analysed and correlated to the different intraoperative findings. RESULTS: Sensorineural hearing loss occurred in a total of 1.3% of 2224 patients with normal preoperative bone conduction thresholds: 0.2% became deaf, 0.8% acquired a high tone loss at 4 kHz and in 0.3% patients also 2 kHz was affected. None of the documented intraoperative complications such as bleeding, unexpected opening of a semicircular canal, extensive manipulation at the ossicular chain or a gusher phenoma showed a relevant effect on postoperative bone conduction thresholds. The incidence of high tone loss was not increased in cases of extensive drilling of the temporal bone. An unexpected opening of the vestibulum led to a small, but statistically significant change in postoperative bone conduction thresholds. CONCLUSIONS: Our results demonstrated that the risk for sensorineural hearing loss caused by middle ear surgery is low. None of the analysed factors seems to be a relevant prognostic risk factor for postoperative inner ear depression.

Adolescent↗
PubMed2005

Specificity of SLC26A4 mutations in the pathogenesis of inner ear malformations.

The traditional hypothesis concerning the pathogenesis of inner ear malformations holds that various types of malformations represent different stages of developmental arrest during embryogenesis. In order to verify this hypothesis, we surveyed mutations in the SLC26A4(PDS) gene, which were documented to cause enlarged vestibular aqueduct (EVA) and Mondini's dysplasia (incomplete partition of the cochlea), in 35 families with various types of inner ear malformations. In 25 families, the probands showed EVA or Mondini's dysplasia as the main temporal bone abnormalities, whereas the probands in the remaining 10 families revealed other types of malformations. In total, 7 mutated SLC26A4 alleles, including 6 missense mutations (A372V, A387V, T410M, S448L, T721M, and H723R) and 1 splice site mutation (IVS7-2A-->G), were detected. All mutated alleles segregated the malformations of EVA and Mondini's dysplasia, whereas no mutated alleles were found in the 10 probands with other types of malformations. SLC26A4 mutations were found in 22 of the 25 probands with EVA or Mondini's dysplasia, indicating that these might be specific to the development of Mondini's dysplasia and EVA. It is inferred that the pathogenetic mechanisms of the various malformations essentially differ, although their radiological findings appear to follow a continuum of morphological changes.

Adolescent↗
PubMed2000

[Tyrosine kinase expression in the inner ear of mice].

Tyrosine-specific phosphorylation events serve to modulate cell to cell interactions during the normal growth and development of many vertebrate tissues. Numerous studies have been performed on the involvement of growth factor receptor tyrosine kinases (RTKs) in inner ear function. Many RTKs, however, have only been recently identified, and their expression patterns have not yet been systematically examined in all tissues. In this study, we surveyed mouse inner ear transcript sequences for the presence of RTKs using a degenerate-PCR based methodology. Isolates encoding RTKs that had and had not been previously identified in the inner ear were obtained. Our data reveals the presence of numerous RTKs in the inner ear that have not yet been studied in the context of inner ear and demonstrates the usefulness of RT-PCR analysis in identifying genes involved in inner ear function.

Animals↗
PubMed2005

[Diagnostic significance of multi-slice computed tomography imaging in congenital inner ear malformations].

OBJECTIVE: To evaluate the feasibility and usability of multi-slice computed tomography (MSCT) in congenital inner ear malformations. METHODS: Fourty-four patients with sensorineural hearing loss (SNHL) were examined by a Somatom Sensation 16 (siemens, Germany) CT scanner with following parameters: 120 kV, 100 mAs, 0.75 mm collimation, 1 mm reconstruction increment, a pitch factor of 1 and a field of view of 100 mm. The axial images of interested ears were reconstructed with 0.1 mm reconstruction increment, and a field of view of 50 mm. The 3D reconstructions were done with volume rendering technique (VRT) on the workstation (3D Virtuoso and Wizard,siemens). RESULTS: Twenty-five patients were normal and 19 patients (36 ears) were congenital inner ear malformations among 44 patients scanned with MSCT. Of the malformations, all the axial, MPR and VRT images can display the site and degree in 33 ears. VRT images were superior to the axial images in displaying the malformations in 3 ears with the small lateral semicircular canal malformations. The malformations were Michel deformity (1 ear), common cavity deformity (3 ears), incomplete partition I (3 ears), incomplete partition II (Mondini deformity, 5 ears), vestibular and semicircular canal malformations( 14 ears), vestibular aqueduct dilate( 16 ears, of which 6 ears accompanied by other malformations), the internal auditory canal malformation(8 ears, all accompanied by other malformations). CONCLUSION: MSCT allows a comprehensively assessing various congenital ear malformations through high quality MPR and VRT reconstructions. VRT images can display the site and degree of the malformations three-dimensionally and intuitionisticly. It is very useful to the cochlear implantation.

Adolescent↗
PubMed1980

Scanning electron microscopic observations on the inner ear of the skate, Raja ocellata.

The inner ear of the skate, Raja ocellata, was examined by scanning electron microscopy. The otolithic membranes have a gelatinous component and an endogenous class of otoconia. Cupulae are reticulate in form. The morphology and polarization of sensory cell hair bundles are described for the various regions of the labyrinth, and are compared with published observations on other species. In the otolithic maculae, the more centrally located receptor cells generally have longer sterecolia than the peripheral cells. The hair bundles of the lacinia are similar to those of the central portion of the sacculus and differed from those of the rest of the utricular macula. Hair bundles in the peripheral regions of all maculae and cristae are similar. The polarization pattern of the utriculus is similar to that of teleosts, while that of the lagena is less clearly dichotomized. The receptor cells of most of the sacculus are oriented in a bivertical direction, with cells in the anterior portion, and a few in the posterior region, being aligned longitudinally. The significance of morphology and polarization with respect to the functions of the otolithic organs is discussed. The relationship of cell processes of the ampullary receptors to the cupula is briefly considered.

Acoustic Maculae↗
PubMed2000

Lack of growth-associated protein-43 reemergence or of growth-associated protein-43 mRNA modulation in deafferented vestibular nuclei during the first 6 weeks after unilateral inner ear lesion.

We investigated whether a unilateral inner ear lesion that destroyed the labyrinthine receptors, the cochlear receptors, and the spiral ganglion induced collateral sprouting in rat vestibular and auditory brainstem nuclei, using growth-associated protein-43 (GAP-43) as an indicator of synaptic remodeling. Both immunocytochemistry and in situ hybridization were performed to detect a potential modulation of GAP-43 and of its messenger RNA (mRNA) at different times after surgery. We failed to observe a reemergence of GAP-43 or a modulation of its mRNA in the deafferented vestibular nuclei at all survival times tested. In contrast, a substantial increase in the expression of GAP-43 was observed in the neuropil of the ipsilateral deafferented cochlear nuclei and in cell bodies of the ipsilateral superior olive. This increase was associated with an up- and downregulation of the mRNA coding for GAP-43 in the ipsilateral ventral cochlear nucleus and in the ipsilateral superior olive, respectively. These data indicate that synaptic remodeling, as assessed by GAP-43 expression, does not seem to occur in the deafferented vestibular complex during the first 6 weeks after labyrinthectomy, whereas it occurs within the first deafferented auditory relays at times as early as 4 days following spiral ganglion and cochlear receptors removal. We conclude that recovery of a normal resting discharge of the deafferented central vestibular neurons and consequently recovery of a normal resting posture and eye position may not depend on collateral sprouting of the remaining vestibular afferents. In contrast, we confirmed that a reactive synaptogenesis occurs in the brainstem auditory nuclei following cochlea and spiral ganglion removal. Its functional significance remains an open question.

Afferent Pathways↗
PubMed1991

Histochemical analysis of glycoconjugates in gelatinous membranes of the gerbil's inner ear.

The gelatinous membranes of the gerbil inner ear were analyzed histochemically for glycoconjugates with a battery of twenty horseradish peroxidase-conjugated lectins. Glycoconjugates with mannose (Man) and/or glucose (Glc), galactose (Gal), fucose (Fuc), N-acetylglucosamine (GlcNAc), N-acetylgalactosamine (GalNAc) and N-acetylneuraminic acid (NeuAc) were detected in the tectorial and otolithic membranes and cupula. Differences in lectin reactivity were observed between tectorial and vestibular membranes and also among zones and between the medial and lateral regions of the middle zone of the tectorial membrane. The distribution of staining differed markedly for several lectins that bind specifically to GalNAc or to GlcNAc but vary in affinity for oligosaccharides containing these sugars in different sequences or linkages. The findings suggest presence of the terminal disaccharides GalNAc alpha 1,3Gal in tectorial membrane and Gal beta 1,3GalNAc in vestibular membranes. Lectin binding profiles provided evidence that the limbal zone's fibrous and attachment layers contain mainly O-glycosidically linked oligosaccharides whereas the middle zone's medial fibrous layer contains both O- and N-linked chains. The remaining regions of the tectorial membrane contain mainly N-linked oligosaccharides with bisected biantennary type chains predominating. Additionally, the marginal band and the middle zone's basal layer contain abundant N-linked oligosaccharides with a triantennary structure.

Animals↗
PubMed2006

Characterization of supporting cell phenotype in the avian inner ear: implications for sensory regeneration.

The avian inner ear possesses a remarkable capacity for the regeneration of sensory receptors after acoustic trauma or ototoxicity. Most replacement hair cells are created by renewed cell division within the sensory epithelium, although some new hair cells may also arise through nonmitotic mechanisms. Current data indicate that epithelial supporting cells play an essential role in regeneration, by serving as progenitor cells. In order to become progenitors, however, supporting cells may need to undergo partial dedifferentiation. In this review, I describe molecules that are expressed by supporting cells in the avian ear. Although a number of these molecules are likely to be critical to the maintenance of the supporting cell phenotype, we presently know very little about phenotypic changes in supporting cells during the early phase of regeneration.

Animals↗
PubMed1999

Evidence for a microglial reaction within the vestibular and cochlear nuclei following inner ear lesion in the rat.

Following unilateral inner ear lesion, astrocytes undergo hypertrophy in the deafferented vestibular and cochlear nuclei as shown by an increase in the level of glial fibrillary acid. The present study extends our understanding of vestibular and cochlear system plasticity by examining microglial changes in these deafferented nuclei. The microglial reaction was studied 1, 2, 4, 8, 14, 21, 28 and 42 days following the lesion with a monoclonal OX-42 antibody and lectins (Griffonia simplicifolia, B4 isolectin) labelled with horseradish peroxidase or fluorescein. The deafferented nuclei were also examined for apoptotic cells by terminal transferase-mediated nick end labelling of nuclear DNA fragments. In control and sham-operated rats, the distribution of the resting microglial cells was uniform in both the vestibular and cochlear nuclei. In the deafferented vestibular complex, the microglial cells increased in number, became hypertrophied and were distributed in the medial, lateral, superior and inferior vestibular nuclei. Reactive microglial cells were also detected in the ipsilateral cochlear nuclei. Some of the immunostained cells were hypertrophic whereas others presented an ameboid morphology with few short and stout processes. The microglial reaction was confined to the antero- and posteroventral cochlear nuclei. Finally, reactive microglia was also observed in the prepositus hypoglossi ipsilateral to the lesion. The microglial reactions within the prepositus hypoglossi, the vestibular and the cochlear nuclei were detectable as early as one day after the lesion and persisted several weeks in both the vestibular and cochlear nuclei. Apoptotic cells were not detected in the vestibular nuclei at any stage following the lesion. In contrast, terminal deoxynucleotidyl transferase-mediated digoxygenin-11-dUTP nick end labelling-positive cells were first detected in the deafferented cochlear nuclei on the 3rd day following the lesion. They reached an apparent maximum by day 8 and then declined until day 24. Double labelling experiments demonstrate that these cochlear terminal deoxynucleotidyl transferase-mediated digoxygenin-11-dUTP nick end labelling-positive cells were also lectin-positive suggesting that reactive cochlear lectin-positive microglia cells were eliminated by a programmed cell death. Our results establish the two experimental models as reliable tools to understand the role of microglia in adult brain plasticity. The cochlear microglial reaction was probably induced by the degeneration of the acoustic nerve which follows the acoustic ganglion destruction. Interestingly, the same reasoning cannot apply to the vestibular microglial reaction following unilateral labyrinthectomy: the vestibular ganglion was spared and the primary vestibular neurons did not degenerate, at least during the first week following the lesion.

Animals↗
PubMedDate not supplied

Electron microscopic study of the inner ear following anaphylaxis.

Although very little is known about the role of immunologic responses in disorders of the inner ear, including sensorineural hearing loss, data lending support to the possibility of their involvement have recently been published. The present experimental study was undertaken to obtain a better understanding of the fine structures of the inner ear following systemic immune responses. In guinea pigs sensitized with egg albumin, antigen challenge not only evoked bronchospasms, but also induced some pathologic changes in the inner ear, especially in the stria vascularis. These findings lead to the inference that the inner ear may be affected by systemic immune responses in sensitized animals.

Anaphylaxis↗
PubMed2004

Temporal bone pathology in hydrocephalus: changes in the inner ear due to increased intracranial pressure.

Changes in the inner ear due to increased intracranial pressure have not yet been clearly defined. We present a postmortem temporal bone study of child with hydrocephalus. The temporal bone was from a 2-year-old female with IVth ventricle ependymoblastoma. In the basal turn of the cochlea, degeneration of the organ of Corti and the nerve ganglion was observed. In the top and middle turn, structures were intact. The utricle and saccule were well preserved. We propose that changes in the inner ear due to increased intracranial pressure begin in the base of the cochlea, and extend to the apex in decreasing degree.

Brain Neoplasms↗