scholarly journals Expression of acetylated tubulin in the postnatal developing mouse cochlea

2018 ◽  
Author(s):  
Wenjing Liu ◽  
Chuanxi Wang ◽  
Hao Yu ◽  
Shaofeng Liu ◽  
Jun Yang
Keyword(s):  
Basilar Membrane ◽  
Stria Vascularis ◽  
Organ Of Corti ◽  
Outer Hair Cells ◽  
Spiral Ligament ◽  
Post Translational Modifications ◽  
Acetylated Tubulin ◽  
Spatiotemporal Expression ◽  
Pillar Cells ◽  
Cochlear Development

Acetylation tubulin is one of the major post-translational modifications of microtubules. Stable microtubules are well known to contain acetylated tubulin. Here, we examined the spatiotemporal expression of acetylated tubulin in the mouse cochlea during postnatal development. At postnatal day 1 (P1), acetylated tubulin was localized primarily to the auditory nerve inside the cochlea and their synaptic contacts with the inner and outer hair cells (IHCs and OHCs). In the organ of Corti, acetylated tubulin occurred first at the apex of pillar cells. At P5, acetylated tubulin first appeared in the phalangeal processes of Deiters’ cells. At P8, staining was maintained in the phalangeal processes of Deiters’ cells. At P10, labeling in Deiters’ cells extended from the apices of OHCs to the basilar membrane. Labeling was expressed throughout the cytoplasm of pillar cells. At P12, acetylated tubulin displayed prominent and homogeneous labeling along the full length of the pillar cells. Linear labeling was present mainly in the Deiters’ cell bodies underlying OHCs. Between P14 and P17, acetylated tubulin was strongly expressed in inner and outer pillar cells and Deiters’ cells in a similar pattern as observed in the adult, and labeling in these cells were arranged in bundles. In addition, acetylated tubulin was intensely expressed in stria vascularis, root cell bodies, and a small number of fibrocytes of the spiral ligament until the adult. In the adult mouse cochlea, immunostaining continued to predominate in Deiters’ cells and pillar cells. Immunolabeling formed cups securing OHCs basal portions, and continued presence of acetylated tubulin-labeled nerve terminals below IHCs was shown. Our results presented here underscored the essential role played by acetylated tubulin in postnatal cochlear development, auditory neurotransmission and cochlear mechanics.

scholarly journals Morphometry of the chinchilla organ of Corti and stria vascularis.

1979 ◽  
Vol 27 (11) ◽  
pp. 1539-1542 ◽  
Author(s):  
P A Santi ◽  
D C Muchow
Keyword(s):  
Morphometric Analysis ◽  
Hair Cells ◽  
Basilar Membrane ◽  
Stria Vascularis ◽  
Organ Of Corti ◽  
Outer Hair Cells

This research describes a procedure for a morphometric analysis of the organ of Corti and stria vascularis in the chinchilla. In nine normal cochleae the length of the basilar membrane and the stria vascularis measured 18.47 and 25.22 mm, respectively. An average of 1910 inner and 7501 outer hair cells were present while an average of 15 inner and 90 outer hair cells were absent. In all cochleae examined there were always some missing hair cells in varying numbers even though the animals had no known ototoxic exposure. Stria area, width and thickness increased from the cochlear apex toward the base. Consistency of changes in stria dimensions among animals was enhanced by expressing position in terms of percentage stria length rather than distance as such. Total stria volume was estimated at 0.15 microliter.

scholarly journals Histopathology of the Human Inner Ear in Alström's Syndrome

2015 ◽  
Vol 20 (4) ◽  
pp. 267-272 ◽  
Author(s):  
Joseph B. Nadol Jr ◽  
Jan D. Marshall ◽  
Roderick T. Bronson
Keyword(s):  
Inner Ear ◽  
Autosomal Recessive ◽  
Ganglion Cells ◽  
Stria Vascularis ◽  
Genetic Disorder ◽  
Spiral Ganglion ◽  
Organ Of Corti ◽  
Outer Hair Cells ◽  
Spiral Ligament ◽  
Human Inner Ear

Alström's syndrome is an autosomal recessive syndromic genetic disorder caused by mutations in the ALMS1 gene. Sensorineural hearing loss occurs in greater than 85% of patients. Histopathology of the inner ear abnormalities in the human has not previously been fully described. Histopathology of the inner ear in Alström's syndrome is presented in 2 genetically confirmed cases. The predominant histopathologic correlates of the sensorineural loss were degeneration of the organ of Corti, both inner and outer hair cells, degeneration of spiral ganglion cells, and atrophy of the stria vascularis and spiral ligament.

Mechanisms of hearing loss and cell death in the cochlea of connexin mutant mice

2020 ◽  
Vol 319 (3) ◽  
pp. C569-C578
Author(s):  
Bei Chen ◽  
Hongen Xu ◽  
Yanfang Mi ◽  
Wei Jiang ◽  
Dan Guo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hearing Loss ◽  
Hair Cell ◽  
Stria Vascularis ◽  
Reactive Oxygen Species Generation ◽  
Cell Loss ◽  
Outer Hair Cells ◽  
Spiral Ligament ◽  
Hair Cell Loss ◽  
Auditory Brain Stem Response

Mutations in connexin 30 (Cx30) are known to cause severe congenital hearing impairment; however, the mechanism by which Cx30 mediates homeostasis of endocochlear gap junctions is unclear. We used a gene deletion mouse model to explore the mechanisms of Cx30 in preventing hearing loss. Our results suggest that despite severe loss of the auditory brain-stem response and endocochlear potential at postnatal day 18, Cx30−/− mice only show sporadic loss of the outer hair cells. This inconsistency in the time course and severity of hearing and hair cell losses in Cx30−/− mice might be explained, in part, by an increase in reactive oxygen species generation beginning at postnatal day 10. The expression of oxidative stress genes was increased in Cx30−/− mice in the stria vascularis, spiral ligament, and organ of Corti. Furthermore, Cx30 deficiency caused mitochondrial dysfunction at postnatal day 18, as assessed by decreased ATP levels and decreased expression of mitochondrial complex I proteins, especially in the stria vascularis. Proteomic analysis further identified 444 proteins that were dysregulated in Cx30−/− mice, including several that are involved in mitochondria electron transport, ATP synthesis, or ion transport. Additionally, proapoptotic proteins, including Bax, Bad, and caspase-3, were upregulated at postnatal day 18, providing a molecular basis to explain the loss of hearing that occurs before hair cell loss. Therefore, our results are consistent with an environment of oxidative stress and mitochondrial damage in the cochlea of Cx30−/− mice that is coincident with hearing loss but precedes hair cell loss.

scholarly journals Vibration of the organ of Corti within the cochlear apex in mice

2014 ◽  
Vol 112 (5) ◽  
pp. 1192-1204 ◽  
Author(s):  
Simon S. Gao ◽  
Rosalie Wang ◽  
Patrick D. Raphael ◽  
Yalda Moayedi ◽  
Andrew K. Groves ◽  
...  
Keyword(s):  
Mechanical Properties ◽  
Phase Difference ◽  
Basilar Membrane ◽  
Organ Of Corti ◽  
Lateral Compartment ◽  
Outer Hair Cells ◽  
Supporting Cells ◽  
Tuning Curves ◽  
Cochlear Amplification

The tonotopic map of the mammalian cochlea is commonly thought to be determined by the passive mechanical properties of the basilar membrane. The other tissues and cells that make up the organ of Corti also have passive mechanical properties; however, their roles are less well understood. In addition, active forces produced by outer hair cells (OHCs) enhance the vibration of the basilar membrane, termed cochlear amplification. Here, we studied how these biomechanical components interact using optical coherence tomography, which permits vibratory measurements within tissue. We measured not only classical basilar membrane tuning curves, but also vibratory responses from the rest of the organ of Corti within the mouse cochlear apex in vivo. As expected, basilar membrane tuning was sharp in live mice and broad in dead mice. Interestingly, the vibratory response of the region lateral to the OHCs, the “lateral compartment,” demonstrated frequency-dependent phase differences relative to the basilar membrane. This was sharply tuned in both live and dead mice. We then measured basilar membrane and lateral compartment vibration in transgenic mice with targeted alterations in cochlear mechanics. Prestin499/499, Prestin−/−, and TectaC1509G/C1509G mice demonstrated no cochlear amplification but maintained the lateral compartment phase difference. In contrast, SfswapTg/Tg mice maintained cochlear amplification but did not demonstrate the lateral compartment phase difference. These data indicate that the organ of Corti has complex micromechanical vibratory characteristics, with passive, yet sharply tuned, vibratory characteristics associated with the supporting cells. These characteristics may tune OHC force generation to produce the sharp frequency selectivity of mammalian hearing.

scholarly journals Expression of Gap Junction Protein Connexin43 in the Adult Rat Cochlea: Comparison with Connexin26

2003 ◽  
Vol 51 (7) ◽  
pp. 903-912 ◽  
Author(s):  
Toshihiro Suzuki ◽  
Tetsuro Takamatsu ◽  
Masahito Oyamada
Keyword(s):  
Gap Junction ◽  
Stria Vascularis ◽  
Three Dimensional ◽  
Organ Of Corti ◽  
Structural Difference ◽  
Lateral Wall ◽  
Spiral Ligament ◽  
Adult Rat ◽  
Junction Protein ◽  
Rat Cochlea

To elucidate whether the two different gap junction proteins connexin43 (Cx43) and connexin26 (Cx26) are expressed and localized in a similar manner in the adult rat cochlea, we performed three-dimensional confocal microscopy using cryosections and surface preparations. In the cochlear lateral wall, Cx43-positive spots were localized mainly in the stria vascularis and only a few spots were present in the spiral ligament, whereas Cx26-positive spots were detected in both the stria vascularis and the spiral ligament. In the spiral limbus, Cx43 was widely distributed, whereas Cx26 was more concentrated on the side facing the scala vestibuli and in the basal portion. In the organ of Corti, Cx43-positive spots were present between the supporting cells but they were fewer and much smaller than those of Cx26. These data demonstrated distinct differences between Cx43 and Cx26 in expression and localization in the cochlea. In addition, the area of overlap of zonula occludens-1 (ZO-1) immunolabeling with Cx43-positive spots was small, whereas it was fairly large with Cx26-positive spots in the cochlear lateral wall, suggesting that the differences are not associated with the structural difference between carboxyl terminals, i.e., those of Cx43 possess sequences for binding to ZO-1, whereas those of Cx26 lack these binding sequences.

scholarly journals Amplification lags nonlinearity in the recovery from reduced endocochlear potential

2020 ◽  
Author(s):  
C. Elliott Strimbu ◽  
Yi Wang ◽  
Elizabeth S. Olson
Keyword(s):  
Hair Cells ◽  
Otoacoustic Emissions ◽  
Basilar Membrane ◽  
Frequency Tuning ◽  
Organ Of Corti ◽  
Endocochlear Potential ◽  
Outer Hair Cells ◽  
Frequency Resolution ◽  
Operating Condition ◽  
Distortion Product

ABSTRACTThe mammalian hearing organ, the cochlea, contains an active amplifier to boost the vibrational response to low level sounds. Hallmarks of this active process are sharp location-dependent frequency tuning and compressive nonlinearity over a wide stimulus range. The amplifier relies on outer hair cell (OHC) generated forces driven in part by the endocochlear potential (EP), the ~ +80 mV potential maintained in scala media, generated by the stria vascularis. We transiently eliminated the EP in vivo by an intravenous injection of furosemide and measured the vibrations of different layers in the cochlea’s organ of Corti using optical coherence tomography. Distortion product otoacoustic emissions (DPOAE) were monitored at the same times. Following the injection, the vibrations of the basilar membrane lost the best frequency (BF) peak and showed broad tuning similar to a passive cochlea. The intra-organ of Corti vibrations measured in the region of the OHCs lost their BF peak and showed low-pass responses, but retained nonlinearity, indicating that OHC electromotility was still operational. Thus, while electromotility is presumably necessary for amplification, its presence is not sufficient for amplification. The BF peak recovered nearly fully within 2 hours, along with a non-monotonic DPOAE recovery that suggests that physical shifts in operating condition are a final step in the recovery process.SIGNIFICANCEThe endocochlear potential, the +80 mV potential difference across the fluid filled compartments of the cochlea, is essential for normal mechanoelectrical transduction, which leads to receptor potentials in the sensory hair cells when they vibrate in response to sound. Intracochlear vibrations are boosted tremendously by an active nonlinear feedback process that endows the cochlea with its healthy sensitivity and frequency resolution. When the endocochlear potential was reduced by an injection of furosemide, the basilar membrane vibrations resembled those of a passive cochlea, with broad tuning and linear scaling. The vibrations in the region of the outer hair cells also lost the tuned peak, but retained nonlinearity at frequencies below the peak, and these sub-BF responses recovered fairly rapidly. Vibration responses at the peak recovered nearly fully over 2 hours. The staged vibration recovery and a similarly staged DPOAE recovery suggests that physical shifts in operating condition are a final step in the process of cochlear recovery.

scholarly journals In vivo optogenetics reveals control of cochlear sensitivity by supporting cells

2021 ◽  
Author(s):  
Victoria Lukashkina ◽  
Snezana Levic ◽  
Patricio Simões ◽  
Zhenhang Xu ◽  
Joseph DiGuiseppi ◽  
...  
Keyword(s):  
Basilar Membrane ◽  
Ex Vivo ◽  
Organ Of Corti ◽  
Outer Hair Cells ◽  
Supporting Cells ◽  
Acoustic Environment ◽  
Cation Conductance ◽  
Fine Control ◽  
Electrical Responses

Abstract Cochlear sensitivity, essential for communication and exploiting the acoustic environment, is due to the sensory-motor outer hair cells (OHCs) that operate in the structural scaffold of supporting cells and extracellular spaces in the cochlear organ of Corti (OoC). It is unclear whether supporting cells (e.g., Deiters cells [DCs] and outer pillar cells [OPCs]) control cochlear sensitivity in vivo. Here we employed optogenetics to measure in vivo sound-induced cochlear mechanical and electrical responses, and ex vivo light-induced DC electrical responses in the OoC of mice that conditionally expressed channelrhodopsins (ChR2) specifically in DCs and OPCs. Illumination activated a nonselective ChR2 cation conductance and depolarized the DCs. This transient action reversibly blocked continuous, normally occurring, minor adjustments of tone-evoked basilar membrane displacements, and OHC voltage responses to tones at and close to their characteristic frequency, and speeded recovery from temporary acoustic desensitization. This is the first direct evidence for the interdependency of the structural, mechanical, and electrochemical arrangement of OHCs and OoC supporting cells which together fine control cochlear sensitivity.

scholarly journals Postnatal Development of Microglia-Like Cells in Mouse Cochlea

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Penghui Chen ◽  
Yongchuan Chai ◽  
Haijin Liu ◽  
Gen Li ◽  
Longhao Wang ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Morphological Changes ◽  
Spiral Ganglion ◽  
Organ Of Corti ◽  
Specific Marker ◽  
Spiral Ligament ◽  
Type I ◽  
Cochlear Inflammation ◽  
Cochlear Development ◽  
The Central Nervous System

Microglial cells are involved in surveillance and cleaning of the central nervous system. Recently, microglial-like cells (MLC) have been found in an adult cochlea and investigated for their role in cochlear inflammation. The presence and potential roles of MLCs during the development of the cochlea, however, remain unclear. In this study, immunostaining was performed using the MLC-specific marker IBA1 to characterize the presence, distribution, and morphology of MLCs in the developing cochlea. From P0 to P14, MLCs were present in a variety of cochlear regions including the modiolus, spiral lamina, spiral ganglion, spiral ligament, and the organ of Corti. Interestingly, the overall number of MLCs in a mouse cochlea steadily increased since P0, peaks at P5, then gradually decreased from P5 to P14. In the spiral ligament, the distribution of the MLCs trends to shift from the type I/II fibrocyte-rich regions to the type III/IV fibrocyte-rich regions during the course of cochlear development, accompanied by the morphological changes of MLCs from the amoeboid, activated form to the ramified, quiescent form. Our results suggested that MLCs experience drastic morphological and distributional changes during postnatal cochlear development, which may play a role in the maturing and remodeling of the cochlea.

Fine Structure Histopathology of Labyrinthitis Ossificans in the Gerbil Model

2005 ◽  
Vol 114 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Steven P. Tinling ◽  
Vishad Nabili ◽  
Hilary A. Brodie
Keyword(s):  
Connective Tissue ◽  
Ganglion Cells ◽  
Stria Vascularis ◽  
Spiral Ganglion ◽  
Organ Of Corti ◽  
Spiral Ligament ◽  
Otic Capsule ◽  
Dense Connective Tissue ◽  
Labyrinthitis Ossificans ◽  
End Stage

Labyrinthitis ossificans (LO) is the pathological deposition of new bone within the lumen of the cochlea and labyrinth. This process occurs most commonly as a result of infection or inflammation affecting the otic capsule. Trauma and vascular compromise can also lead to neo-ossification within the otic capsule. The mechanism that regulates this process remains unestablished. This study details the end-stage histopathology in high-resolution plastic thin sections. Twenty Mongolian gerbils were infected by intrathecal injection of Streptococcus pneumoniae type 3 followed by subcutaneous penicillin G procaine (8 days) and were painlessly sacrificed 3 months later. The cochleas were serially divided and sectioned for light and electron microscopy. Sixteen of 20 animals (27 of 40 cochleas) demonstrated LO. Cochlear damage was most extensive in the vestibule and basal turn and decreased toward the apex, which often appeared normal. The histopathologic findings consisted of 1) new bone, calcospherites, osteoid, and fibrosis without dense connective tissue or osteoblasts extending from the endosteal wall into the lumen of the vestibule and scala tympani; 2) areas of dense connective tissue and osteoid enclosed by epithelial cells conjoined with the organ of Corti, stria vascularis, spiral ligament, and vestibular (Reissner's) membrane; and 3) partial to complete loss of the organ of Corti, spiral ligament cell bodies, stria vascularis, and spiral ganglion cells. Osteoblastic activity was not demonstrated in end-stage ossification in LO in the gerbil model. Neoossification appears to occur by calcospherite deposition along collagen-like fibrils within osteoid. The destruction of the organ of Corti, spiral ganglion cells, stria vascularis, and cells of Reissner's membrane and the spiral ligament occurs even in the absence of ossification of the cochlear duct.

scholarly journals NTPDase1 and NTPDase2 Immunolocalization in Mouse Cochlea: Implications for Regulation of P2 Receptor Signaling

2002 ◽  
Vol 50 (11) ◽  
pp. 1435-1441 ◽  
Author(s):  
Srdjan M. Vlajkovic ◽  
Peter R. Thorne ◽  
Jean Sévigny ◽  
Simon C. Robson ◽  
Gary D. Housley
Keyword(s):  
Hair Cells ◽  
Spiral Ganglion ◽  
Organ Of Corti ◽  
Nerve Fibers ◽  
Outer Hair Cells ◽  
Spiral Ligament ◽  
Receptor Signaling ◽  
P2 Receptor ◽  
Efferent Nerve ◽  
Root Region

Cellular, molecular, and physiological studies have demonstrated an important signaling role for ATP and related nucleotides acting via P2 receptors in the cochlea of the inner ear. Signal modulation is facilitated by ectonucleotidases, a heterologous family of surface-located enzymes involved in extracellular nucleotide hydrolysis. Our previous studies have implicated CD39/NTPDase1 and CD39L1/NTPDase2, members of the ectonucleoside triphosphate diphosphohydrolase (E-NTPDase) family, as major ATP-hydrolyzing enzymes in the tissues lining the cochlear endolymphatic and perilymphatic compartments. NTPDase1 hydrolyzes both nucleoside triphosphates and diphosphates. In contrast, NTPDase2 is a preferential nucleoside triphosphatase. This study characterizes expression of these E-NTPDases in the mouse cochlea by immunohistochemistry. NTPDase1 can be immunolocalized to the cochlear vasculature and neural tissues (primary auditory neurons in the spiral ganglion). In contrast, NTPDase2 immunolabeling was principally localized to synaptic regions of the sensory inner and outer hair cells, stereocilia and cuticular plates of the outer hair cells, supporting cells of the organ of Corti (Deiters’ cells and inner border cells), efferent nerve fibers located in the intraganglionic spiral bundle, and in the outer sulcus and root region of the spiral ligament. This differential expression of NTPDase1 and 2 in the cochlea suggests spatial regulation of P2 receptor signaling, potentially involving different nucleotide species and hydrolysis kinetics.

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