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PubMed2002

Fibroblast growth factor signaling regulates pillar cell development in the organ of corti.

One of the most striking aspects of the cellular pattern within the sensory epithelium of the mammalian cochlea is the presence of two rows of pillar cells in the region between the single row of inner hair cells and the first row of outer hair cells. The factors that regulate pillar cell development have not been determined; however, previous results suggested a key role for fibroblast growth factor receptor 3 (FGFR3). To examine the specific effects of FGFR3 on pillar cell development, we inhibited receptor activation in embryonic cochlear explant cultures. Results indicated that differentiation of pillar cells is dependent on continuous activation of FGFR3. Moreover, transient inhibition of FGFR3 did not inhibit the pillar cell fate permanently, because reactivation of FGFR3 resulted in the resumption of pillar cell differentiation. The effects of increased FGFR3 activation were determined by exposing cochlear explants to FGF2, a strong ligand for several FGF receptors. Treatment with FGF2 led to a significant increase in the number of pillar cells and to a small increase in the number of inner hair cells. These effects were not dependent on cellular proliferation, suggesting that additional pillar cells and inner hair cells were a result of increased recruitment into the prosensory domain. These results indicate that FGF signaling plays a critical role in the commitment and differentiation of pillar cells. Moreover, the position of the pillar cells appears to be determined by the activation of FGFR3 in a subset of the progenitor cells that initially express this receptor.

Animals↗
PubMed1994

Choline-acetyltransferase-like immunoreactivity in the organ of Corti of the rat during postnatal development.

The mammalian cochlea receives efferent innervation from neurons located in the superior olivary complex. This efferent olivocochlear innervation is divided in two separate systems, lateral and medial, which mainly innervate afferent dendrites connected to inner hair cells and the cell body of outer hair cells, respectively. Besides other substances, lateral and medial efferent terminals of the adult cochlea use acetylcholine (ACh) as a neurotransmitter. In this study, we have used immunocytochemistry to detect the presence of choline acetyltransferase (ChAT), the synthesizing enzyme of ACh, in efferent olivocochlear terminals during the development of the rat. The appearance and distribution of immunoreactivity to ChAT has been studied in developing rat cochleas from birth (postnatal day 1, P1) to adulthood. Attention was paid to the temporal relationships between the expression of ChAT, the presence of other putative neuroactive substances, the onset of hearing and other developmental phenomena. Our results indicate that ChAT-like immunoreactivity is already present at birth (P1) in the region of inner hair cells, that it appears at P3 in the outer hair cell area and that it reaches an adult pattern of distribution by P15. ACh may thus be present early in the developing cochlea, before the onset of hearing, as it also occurs with other putative transmitters/modulators such as enkephalins, CGRP or GABA. It is suggested that ACh could be involved in the modulation of sound-evoked potentials as soon as they appear, and in the regulation of other developmental phenomena such as neurite outgrowth or synaptogenesis.

Aging↗
PubMed2002

Cysteine-string protein in inner hair cells of the organ of Corti: synaptic expression and upregulation at the onset of hearing.

Cysteine-string protein is a vesicle-associated protein that plays a vital function in neurotransmitter release. We have studied its expression and regulation during cochlear maturation. Both the mRNA and the protein were found in primary auditory neurons and the sensory inner hair cells. More importantly, cysteine-string protein was localized on synaptic vesicles associated with the synaptic ribbon in inner hair cells and with presynaptic differentiations in lateral and medial olivocochlear terminals -- the cell bodies of which lie in the auditory brainstem. No cysteine-string protein was expressed by the sensory outer hair cells suggesting that the distinct functions of the two cochlear hair cell types imply different mechanisms of neurotransmitter release. In developmental studies in the rat, we observed that cysteine-string protein was present beneath the inner hair cells at birth and beneath outer hair cells by postnatal day 2 only. We found no expression in the inner hair cells before about postnatal day 12, which corresponds to the period during which the first cochlear action potentials could be recorded. In conclusion, the close association of cysteine-string protein with synaptic vesicles tethered to synaptic ribbons in inner hair cells and its synchronized expression with the appearance and maturation of the cochlear potentials strongly suggest that this protein plays a fundamental role in sound-evoked glutamate release by inner hair cells. This also suggests that this role may be common to ribbon synapses and conventional central nervous system synapses.

Aging↗
PubMedDate not supplied

A temporospatial map of adhesive molecules in the organ of Corti of the mouse cochlea.

In the nervous system, several classes of cell-surface and extracellular matrix molecules have been implicated in processes such as neural growth, fasciculation, pathfinding, target recognition and synaptogenesis, which require cell-to-cell or cell-to-substrate binding. In the developing mouse cochlea, little is known about the types of cell-surface and extracellular matrix molecules existing along the neural growth paths or their possible roles in development. Whole mount and sectioned cochlear tissue were immunolabeled for six different adhesive molecules - neural cell adhesion molecule (NCAM), polysialic acid (PSA), neural cell adhesion molecule L1, E-cadherin, syndecan-1 and tenascin-C. A temporospatial map of adhesive molecule distribution in the basal turns of the mouse cochlea was generated. Distributions of adhesive molecules were compared to each other and to the known progress of neural development in the region. This comparison demonstrated differences in the complements of adhesive molecules between the inner and outer hair cell regions, and variations in the expressions of adhesion molecules among different types of nerve fibers. In addition, developmental changes in the adhesive environment around and beneath the outer hair cells coincided with the known timing of the appearance of morphologically defined efferent synapses. These observations raise the possibility that molecular differences at the cell surface of inner and outer hair cells are one way that ingrowing neurites distinguish different environments to determine their growth routes and synaptic partners in the cochlea. In addition these observations demonstrate the potential for differential signaling of afferent and efferent innervation by altering the microenvironments in which synapses are formed.

Animals↗
PubMed2006

Chlorpromazine alters cochlear mechanics and amplification: in vivo evidence for a role of stiffness modulation in the organ of corti.

Although prestin-mediated outer hair cell (OHC) electromotility provides mechanical force for sound amplification in the mammalian cochlea, proper OHC stiffness is required to maintain normal electromotility and to transmit mechanical force to the basilar membrane (BM). To investigate the in vivo role of OHC stiffness in cochlear amplification, chlorpromazine (CPZ), an antipsychotic drug that alters OHC lateral wall biophysics, was infused into the cochleae in living guinea pigs. The effects of CPZ on cochlear amplification and OHC electromotility were observed by measuring the acoustically and electrically evoked BM motions. CPZ significantly reduced cochlear amplification as measured by a decline of the acoustically evoked BM motion near the best frequency (BF) accompanied by a loss of nonlinearity and broadened tuning. It also substantially reduced electrically evoked BM vibration near the BF and at frequencies above BF (< or =80 kHz). The high-frequency notch (near 50 kHz) in the electrically evoked BM response shifted toward higher frequency in a CPZ concentration-dependent manner with a corresponding phase change. In contrast, salicylate resulted in a shift in this notch toward lower frequency. These results indicate that CPZ reduces OHC-mediated cochlear amplification probably via its effects on the mechanics of the OHC plasma membrane rather than via a direct effect on the OHC motor, prestin. Through modeling, we propose that with a combined OHC somatic and hair bundle forcing, the upward-shift of the approximately 50-kHz notch in the electrically-evoked BM motion may indicate stiffness increase of the OHCs that is responsible for the reduced cochlear amplification.

Acoustic Stimulation↗
PubMedDate not supplied

Apoptosis of inner hair cells caused by laser ablation of their spiral ganglion neurons in cultures of the mouse organ of Corti.

Laser beam ablation of spiral ganglion neurons was performed in seven organotypic cultures of the newborn mouse cochlea between 5 and 8 days in vitro, with a recovery period of from 18 hours to 3 days. Direct somatic injury (laser or mechanical) inflicted on hair cells does not necessarily cause their death; many of them survive, repair damage and re-establish their neurosensory connections. By contrast, laser irradiation and ablation of their afferent spiral ganglion neurons causes a most spectacular degeneration of sensory cells within 18-48 hours after the insult. Ultrastructurally, the degenerated hair cells-characteristically the inner hair cells-display "dark-cell vacuolar degeneration" that combines the signs of apoptotic death (the peripheral condensation of nuclear chromatin and nuclear pyknosis) with signs of cell edema, vacuolization and necrosis. The ultimate condensation of the cytoplasm gives the dead cells a jet black appearance. The irradiated spiral ganglion neurons die displaying similar pathological characteristics. The extent and locus of inner hair cell degeneration correspond to that of ablated spiral ganglion neurons: ultimately the ablation of one neuron causes degeneration of a single inner hair cell within the closest radial segment of the afferent innervation. The elimination of spiral ganglion neurons by mechanical means does not affect hair cell survival. It is inferred that the laser pulse acts as a stimulus depolarizing the neuronal membrane of the spiral ganglion neurons and their radial fibers and causing the excitotoxic death of their synaptic sensory cells through excessive stimulation of the glutamatergic receptors. Reciprocal pre-and postsynaptic synapses between the afferent dendrites and inner hair cells in culture could possibly serve as entryways of the stimulus. The pathogenesis of this apparent transsynaptically-induced apoptotic death of inner hair cells will be further examined in culture.

Animals↗
PubMed1993

Evidence for calcium-binding proteins and calcium-dependent regulatory proteins in sensory cells of the organ of Corti.

Calcium is thought to play a major signaling role in outer hair cells to control metabolism, cytoskeletal integrity, cell shape and cell excitability. For this to happen, in resting cells the concentration of free calcium ions must be maintained at low levels so that focal increases can trigger specific events. In this paper, the localization of calcium, calcium-binding and calcium-dependent regulatory proteins in sensory cells from the guinea pig inner ear was demonstrated using immunocytochemical and histochemical techniques. We found the calcium buffer and/or calcium sensor proteins calmodulin, calbindin and calsequestrin predominantly in sensory cells and that when present, these proteins can be enriched in the outer hair cells. Calmodulin is found in the stereocilia, in the cuticular plate and in the cytoplasm and calbindin is found only in the cuticular plate and cytoplasm of both the inner and outer hair cells. The staining for these proteins in the outer hair cells is homogeneous, with no apparent compartmentalization along the lateral wall. Calsequestrin, thought to store and release calcium from membrane bound intracellular storage sites is found only in the cytoplasm of outer hair cells. There, it has a more punctuate staining pattern than does calmodulin or calbindin suggesting that it may be present in calciosomes rather than soluble in the cytoplasm. We did not detect caldesmon and S-100. Using the potassium pyroantimonate technique, we found precipitates containing calcium ions distributed throughout the cytoplasm of outer hair cells, with no evidence that the subsurface cisterns along the lateral wall act as calcium storage sites. Thus, calcium in resting cells is found in the cytoplasm along with calbindin and calmodulin and appears to have a punctate distribution consistent with a co-localization with calsequestrin. The implications of this distribution with respect to the slow shortening and elongation seen in outer hair cells are discussed.

Animals↗
PubMedDate not supplied

Cisplatin ototoxicity involves organ of Corti, stria vascularis and spiral ganglion: modulation by alphaMSH and ORG 2766.

It has been shown that alphaMSH and the nonmelanotropic ACTH/MSH(4-9) analog ORG 2766 can ameliorate cisplatin-induced neurotoxicity and ototoxicity. Here, we investigated whether these peptides delay the occurrence of the cisplatin-induced shift in auditory threshold, and whether they affect the subsequent recovery of cochlear potentials. Chronically implanted round window electrodes were used to obtain daily recordings of auditory nerve compound action potentials (CAP) and cochlear microphonics at frequencies ranging from 2 to 16 kHz. Cisplatin (1.5 mg/kg i.p.) plus alphaMSH, ORG 2766 (75 mug/kg s.c.), or saline were injected daily until the 40-dB CAP threshold shift at 8 kHz was reached. Endocochlear potential (EP) was measured either 1-2 days or 28 days later, followed by morphometric analysis of the cochlea. Peptide cotreatment did not consistently delay the threshold shift; however, the CAP threshold recovered faster and to a greater extent, with the potency order being alphaMSH > ORG 2766 > saline. Significant recovery at the 2 highest frequencies was seen in the alphaMSH-treated animals only. CAP amplitude at high sound pressures, which depends more on nerve function than on outer hair cell (OHC) function, decreased severely in all groups but recovered significantly in the alphaMSH- and completely in the ORG-2766-cotreated group. EP was significantly lower in the first days after the threshold shift but had completely recovered at 28 days. Morphometric analysis of the spiral ganglion also indicated involvement of ganglion cells. OHC loss was most severe in the basal turn of saline-cotreated animals. These data suggest that the cisplatin-induced acute threshold shift might be due to reversible strial failure, whereas subsequent OHC survival determines the final degree of functional recovery. Both OHC loss and neuronal function were ameliorated by peptide cotreatment.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Correlation of otosclerotic foci and degenerative changes in the organ of Corti and spiral ganglion.

Statistical analyses of histopathologic findings in the cochlea and spiral ganglion of 37 temporal bones with otosclerosis, 12 controls of similar age, and seven controls with normal hearing were performed. In temporal bones with otosclerosis there was significant atrophy of the spiral ligament and stria vascularis in regions with endosteal involvement by otosclerosis, compared with regions without endosteal involvement (P less than .0001). There was more generalized atrophy of the stria vascularis in cochleae with two or more sites of endosteal involvement by otosclerosis than in cochleae with only one site of endosteal involvement (P less than .02), cochleae in temporal bones with otosclerosis but without endosteal involvement (P less than .05), or cochleae of controls of similar age (P less than .007). In addition, there was more atrophy of the spiral ligament in cochleae with two or more sites of endosteal involvement than in cochleae of similar age from the control group (P less than .03). In temporal bones with otosclerosis, there was no significant difference in counts of outer hair cells and density of spiral ganglion cells between regions demonstrating endosteal involvement by otosclerosis and regions without such involvement. However, total outer hair cell counts were lower in cochleae with two or more sites of endosteal involvement of otosclerosis than in cochleae with one site of endosteal involvement (P less than .04), cochleae in temporal bones with otosclerosis but without endosteal involvement (P less than .02), or cochleae from individuals of similar age but without otosclerosis (P = .05). Comparison of the mean bone conduction threshold, as measured in life, in temporal bones with otosclerosis compared with the air conduction threshold in aged-matched controls, demonstrated that only cochleae with two or more sites of endosteal involvement had a mild but statistically significant (P = .05) decrease in hearing. There was no evidence to support the concept that otosclerotic foci without stapedial fixation frequently cause significant degeneration of the cochlea or elevation of bone conduction thresholds.

Adolescent↗
PubMed2002

Caffeine and ryanodine demonstrate a role for the ryanodine receptor in the organ of Corti.

The hypothesis that the release of Ca(2+) from ryanodine receptor activated Ca(2+) stores in vivo can affect the function of the cochlea was tested by examining the effects of caffeine (1-10 mM) and ryanodine (1-333 microM), two drugs that release Ca(2+) from these intracellular stores. The drugs were infused into the perilymph compartment of the guinea pig cochlea while sound (10 kHz) evoked cochlear potentials and distortion product otoacoustic emissions (DPOAEs; 2f(1)-f(2)=8 kHz, f(2)=12 kHz) were monitored. Caffeine significantly suppressed the compound action potential of the auditory nerve (CAP) at low intensity (56 dB SPL; 3.3 and 10 mM) and high intensity (92 dB SPL; 10 mM), increased N1 latency at high and low intensity (3 and 10 mM) and suppressed low intensity summating potential (SP; 10 mM) without an effect on high intensity SP. Ryanodine significantly suppressed the CAP at low intensity (100 and 333 microM) and at high intensity (333 microM), increased N1 latency at low intensity (33, 100 and 333 microM) and at high intensity (333 microM) and suppressed low intensity SP (100 and 333 microM) and increased high intensity SP (333 microM). The cochlear microphonic (CM) evoked by 10 kHz tone bursts was not affected by caffeine at high or low intensity, and ryanodine had no effect on it at low intensity but decreased it at high intensity (10, 33, 100 and 333 microM). In contrast, caffeine (10 mM) and ryanodine (33 and 100 microM) significantly increased CM evoked by l kHz tone bursts and recorded from the round window. Caffeine (10 mM) and ryanodine (100 microM) reversibly suppressed the cubic DPOAEs evoked by low intensity primaries. Overall, low intensity evoked responses were more sensitive and were suppressed to a greater extent by both drugs. This is consistent with the hypothesis that release of Ca(2+) from ryanodine receptor Ca(2+) stores, possibly in outer hair cells and supporting cells, affects the function of the cochlear amplifier.

Action Potentials↗
PubMed2002

Influence of neurotrophins on the synaptogenesis of inner hair cells in the deaf Bronx waltzer (bv) mouse organ of Corti in culture.

UNLABELLED: The Bronx waltzer (bv) deaf mouse is characterized by massive degeneration of the primary auditory receptors, the inner hair cells, which occurs during the time of expected afferent synaptogenesis. The process is associated with degeneration and protracted division of the normally postmitotic afferent spiral ganglion neurons. To investigate the potential role of neurotrophins in the afferent synaptogenesis of inner hair cells, we exposed bv newborn cochleas in organotypic culture to brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and nerve growth factor (NGF), and also to gamma aminobutyric acid (GABA), for up to 8 days. The study was done using light and electron microscopy. Only about 20% of the inner hair cells survived in culture, regardless of the treatment, similar to the number in the intact mutant in our colony. Depending on the exogenous treatment, this population consisted of either innervated ultrastructurally normal cells or denervated dedifferentiated cells wrapped-in lieu of nerve endings-by the supporting inner phalangeal and border cells. In the control and GABA cultures, inner hair cells were mostly denervated. BDNF and NT-3 alone or combined increased synaptogenesis and hair cell survival only during the first 3 days (by about 10%); however, the cells became denervated by 8 postnatal (PN). Only NGF induced stable innervation and differentiation of neurosensory relationships, including supernumerary innervation characteristic of the intact bv. Denervation among the remaining 20% of inner hair cells induced a reactive wrapping by inner phalangeal and border cells which evidently extended inner hair cell survival. Immunocytochemical studies of these reactive supporting cells were done in the intact (8 PN) mutant cochlea. The supporting cells that provide sustenance to the denervated inner hair cells displayed strong BDNF (and possibly NT-3) immunoreactivity. Subsequently, we revealed the presence of all three neurotrophins in the inner hair cell region of the developing (1-8 PN) cochlea of the normal ICR mouse. The inner hair cells expressed all three neurotrophins; BDNF prevailed in the inner phalangeal cells, NT-3 in the pillar cells and inner phalangeal cells, and NGF in the pillar cells. IN CONCLUSION: initially, the 80% loss of inner hair cells is apparently caused by their failed afferent synaptogenesis. Exogenous neurotrophins influence synaptogenesis in the bv in culture, but NGF alone is successful in promoting stable neurosensory relationships. The presence of neurotrophins in supporting cells in the normal and degenerating cochlea indicates their role in the sustenance of inner hair cells.

Aging↗
PubMed2002

In vitro activation of extracellular signal-regulated kinase1/2 in the inner ear of guinea pigs.

Growth factors such as vascular endothelial growth factor (VEGF) exert their proliferative properties partly through activation of mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK1/2). Although both VEGF and inactive ERK could be detected in the inner ear of guinea pigs, under normal conditions activated ERK (phospho-ERK) was found only sparely. Cochleae of adult guinea pigs were removed, incubated with VEGF in a carbogen-gased organ-bath for 5, 15, 30 and 60 min (n=6 in each group), fixed with PFA 4%, embedded in paraffin and sectioned, followed by immunohistochemical staining to inactive and active ERK. Whereas inactive ERK was found in all cochleae, in sensory and supporting cells of the apex activated ERK was strongly detected after 5-min VEGF-incubation. After 15 min all Corti-organs showed clear staining corresponding to activated ERK, which decreased again after 30 min. Faint staining in endothelial cells of the spring-coil-vessels and in the spiral ganglion cells was found after 30 min and was increased after 60 min, while the staining in the Corti-organs vanished. Addition of the MEK-inhibitor PD 98059 to the organ-bath led to diminished phospho-ERK1/2 immunostaining. These findings provide evidence for a VEGF-dependent phosphorylation of ERK1/2 in the cochlea. Activated ERK1/2 is thought to support axonal outgrowth, enhancement of cell survival and to regulate the turnover of the NO/cGMP-pathway.

Animals↗
PubMed2003

Reciprocal synapses between inner hair cell spines and afferent dendrites in the organ of corti of the mouse.

We provide, for the first time, ultrastructural evidence for the differentiation of reciprocal synapses between afferent dendrites of spiral ganglion neurons and inner hair cells. Cochlear synaptogenesis of inner hair cells in the mouse occurs in two phases: before and after the onset of hearing at 9-10 postnatal (PN) days. In the first phase, inner hair cells acquire afferent innervation (1-5 PN). Reciprocal synapses form around 9-10 PN on spinous processes emitted by inner hair cells into the dendritic terminals, predominantly in conjunction with ribbon afferent synapses. During the second phase, which lasts up to 14 PN, synaptogenesis is led by the olivocochlear fibers of the lateral bundle, which induce the formation of compound and spinous synapses. The afferent dendrites themselves also develop recurrent presynaptic spines or form mounds of synaptic vesicles apposed directly across inner hair cell ribbon synapses. Thus, in the adult 2-month mouse, afferent dendrites of spiral ganglion neurons are not only postsynaptic but also presynaptic to inner hair cells, providing a synaptic loop for an immediate feedback response. Reciprocal synapses, together with triadic, converging, and serial synapses, are an integral part of the afferent ribbon synapse complex. We define the neuronal circuitry of the inner hair cell and propose that these minicircuits form synaptic trains that provide the neurological basis for local cochlear encoding of the initial acoustic signals.

Afferent Pathways↗
PubMed1980

[Effect of a 6-week vitamin A-deficient diet on the sensory cells of the inner ear. Light and electron microscopic studies].

Histologic studies of the inner ear in rats with chronic vitamin A deficiency have produced contradicting results. In our own electronmicroscope investigations of the inner ear of young rats after a six week vitamin A deficit diet we found a lacking of the cuticle in the outer hair cells and a subtotally lacking of the cuticle in the inner hair cells. Furthermore, we found changes in the reticular system of the intermediate zone. These morphologic changes together with the recent findings of high concentrations of vitamin A in the corti organ support the hypothesis that the acoustic sensory receptors contain or functionally depend upon vitamin A.

Animals↗
PubMed1998

Tunnel crossing fibers and their synaptic connections within the inner hair cell region in the organ of corti in the maturing mouse.

Combined ultrastructural and immunocytochemical studies reveal that in the adolescent 12- to 17-day-old mouse the afferent tunnel crossing fibers that innervate outer hair cells receive synaptic contacts from three distinct sources: the GABAergic fibers (GABA = gamma-aminobutyric acid) of the lateral olivocochlear bundle, the non-GABAergic efferent tunnel crossing fibers, and the inner hair cells themselves. The GABAergic fibers give off collaterals that synapse with the afferent tunnel fibers as they cross the inner hair cell region. These collaterals also form synapses with afferent radial dendrites that are synaptically engaged with the inner hair cells. Vesiculated varicosities of non-GABAergic efferent tunnel fibers also synapse upon the outer spiral afferents. Most of this synaptic activity occurs within the inner pillar bundle. Distinctive for this region are synaptic aggregations in which several neuronal elements and inner hair cells are sequentially interconnected. Finally, most unexpected were the afferent ribbon synapses that inner hair cells-formed en passant on the shafts of the apparent afferent tunnel fibers. The findings indicate that: (1) the afferent tunnel (i.e., outer spiral) fibers may be postsynaptic to both the inner and the outer hair cells; (2) the non-GABAergic efferent and the afferent tunnel fibers form extensive synaptic connections before exiting the inner pillar bundle; (3) the GABAergic component of the lateral olivocochlear system modulates synaptically both radial and outer spiral afferents.

Age Factors↗
PubMed1984

Cross-links between stereocilia in the guinea pig organ of Corti, and their possible relation to sensory transduction.

Hair cells of the guinea pig cochlea were preserved for electron microscopic examination by fixing in glutaraldehyde without the use of osmium. An extensive array of cross-links was seen between the stereocilia, by both scanning and transmission electron microscopy. The stereocilia were linked together laterally, particularly near their apical ends, by links running approximately at right angles to the long axis of the stereocilia. One set joined stereocilia of the same row, and another set joined stereocilia of the different rows, holding the tips of the shorter stereocilia in towards the longer stereocilia of the next row. In addition, the tip of each shorter stereocilium on the hair cell gave rise to a single, upwards-pointing link, which ran up to join the taller stereocilium of the next row. We suggest that distortion of this link would give rise to sensory transduction. On this basis, we are able to explain the V shape of the rows of stereocilia on outer hair cells. Within the rows, the three-dimensional arrangement of the stereocilia was different from that seen conventionally. Rather than standing parallel, the stereocilia of the different rows tapered in together at the tips, presumably held by the laterally-running cross-links. In addition, a membrane roughness, particularly pronounced in the region of the stereocilium which gives rise to the cross-links, was seen. However, the lateral and basal surface membranes of the hair cell, and the membranes of the internal organelles, had a more conventional appearance.

Animals↗
PubMed1994

Differences of inner and outer hair cells in the organ of Corti of the guinea pig in respect to the cellular content of precipitable calcium.

Differences between inner and outer hair cells in the cellular content of precipitable calcium were detected using a potassium pyroantimonate precipitation method and the electron spectroscopic imaging (ESI-) technique. The cytoplasm of the inner hair cells was scattered with a high number of calcium precipitates in all analysed animals, but only a few reaction products could be identified in the cytoplasm of the outer hair cells in all analyzed specimens. Even the well developed system of the subsurface fenestrated cisternae in the outer hair cells was nearly empty of calcium precipitates. A relatively high amount of reaction products could be identified in the nuclei of both types of nerve endings of the receptor cells. Significant differences regarding the content of precipitable calcium were found in the different types of nerve endings, which come into contact with the basal parts of both receptor cells. The observed differences in the content of precipitable calcium between the two types of hair cells are discussed with respect to their probable different roles in signal transduction processes.

Animals↗