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PubMed1995

Luminal non-selective cation and outwardly rectifying chloride channels in cultured strial marginal cells from gerbil.

Ionic channels located on the luminal side of strial marginal cells (MCs) of gerbil in culture were investigated using the patch-clamp technique. Two types of channels were identified. The most frequently recorded single-channel activity corresponded to a non-selective cation (NSC) channel with a conductance of 23.7 +/- 0.2 pS (n = 18) in symmetrical NaCl conditions. The channel was activated by internal Ca2+ and inhibited by internal adenine nucleotides and flufenamic acid. Spontaneous activity of NSC channels was found in 16% of the cell-attached patches and with a very high density (9 +/- 2 levels/patch, n = 28) in 100% of the excised patches. An outwardly rectifying chloride (ORC) channel was also identified in 14% of the patches but only after excision. The channel exhibited at 0 mV a unit conductance of 26.8 +/- 1.3 pS (n = 8) and a strong outward rectification in symmetrical NaCl conditions, and the open probability increased with depolarization. The luminal NSC channel and the ORC channel evidenced in this study might participate in the production of endolymph. Although extrapolation of the presents results to the in vivo situation should be made with caution, this study suggests that culture of strial MCs may be a suitable model for investigation of endolymph physiology.

Adenine Nucleotides↗
PubMed2006

Endocytosis of microperoxidase in the marginal cells of stria vascularis.

OBJECTIVE: Endocytosis has been thought to control entry into the cell and play a crucial role in the development, immune response, neurotransmission, intercellular communication, signal transduction, and cellular and organismal homeostasis. We investigated the basic properties of endocytosis in the marginal cells of stria vascularis (SV) to discuss whether marginal cells have a potential to maintain the endolymph homeostasis. METHODS: We perfused microperoxidase (MPO), an endocytosis tracer, into the cochlear duct. After 5-60 min of endolymphatic perfusion, the tissues were fixed and the distribution of MPO within the marginal cell was observed by transmission electron microscopy. RESULTS: Endocytosis started already at 5 min after MPO perfusion. Small MPO-loaded endosomes were observed up to 30 min after MPO perfusion. The small tubulovesicular endosomes and the plasma membrane invagination were not decorated by an electron dense bristle structure. After endocytosis, MPO labeled preendosomes were quickly transported to the large vacuolar endosomes that connected with tubular endosomes. At 60 min after MPO perfusion, MPO-loaded large vesicles that have small vesicles in the lumen were observed. CONCLUSION: The time-course of MPO-loaded endosomes was similar to that of CF-loaded endosomes in the marginal cells of SV. The strial marginal cells have vigorous endocytotic activity both in clathrin-independent and clathrin-dependent endocytosis. This high activity of endocytosis in SV seems to be needed to maintain the homeostasis of endolymph via membranous channels and/or receptors regulations.

Animals↗
PubMed2006

Assembly of the otoconia complex to the macular sensory epithelium of the vestibule.

In the inner ear, specificity of stimulus perception is achieved by associating the sensory epithelia of the three mechanoreceptor organs, the utricle/saccule, cristae, and cochlea, with distinct types of acellular matrices. Only the utricle and saccule have an extremely dense matrix, the otoconial complex, which overlies the sensory epithelium (macula) and provides inertial mass to generate shearing forces essential for the mechanoreceptors to sense gravity and linear acceleration. Such sensation is necessary for spatial orientation and balance. The importance of otoconia is clearly demonstrated by the impact of balance disorders upon the elderly population that involve otoconia degeneration, as well as by canalithiasis and cupulolithiasis, in which otoconia are dislocated. This underscores the need to understand how otoconia are formed and maintained and how to prevent their degeneration. To date, a number of otoconia-related proteins have been identified mostly in mice and bony fish. Although most of these proteins are also present in other structures of the inner ear, a distinct collection of proteins in the macula plus the unique ionic microenvironment of the endolymph near its epithelium likely contribute to the site-specific calcification of otoconia. Based on the current literature and ongoing research, this mini-review postulates a working model of how the otoconia complex is assembled specifically above the macular sensory epithelium of the vestibule. The central hypothesis of this model is that proteins are critical in sequestering calcium for crystallization in the calcium-poor endolymph. The review also sets forth some issues that need to be resolved in the future.

Animals↗
PubMed1998

Interaction of methylprednisolone and transient asphyxia on the inner ear of the adrenalectomized rat.

Methylprednisolone has been shown clinically to have beneficial effects on certain types of hearing loss. In the current study, compound action potential (CAP) thresholds, endocochlear potentials (EPs), and potassium concentration (CK+) values in the endolymph were determined under conditions of transient asphyxia (45 seconds) and methylprednisolone treatment (24 hours) in bilateral adrenalectomized rats. Treatment with methylprednisolone significantly reduced the effect of transient asphyxia on CAP thresholds as compared with nontreated animals. Methylprednisolone did not alter the dramatic short-term reduction in the EPs produced by anoxia. Potassium concentrations in treated adrenalectomized rats were significantly lower before transient asphyxia than in nontreated adrenalectomized rats. In the nontreated rats, transient asphyxia induced a reduction in CK+ levels that was not seen in the methylprednisolone-treated animals. The data support the clinical application of methylprednisolone for certain forms of hearing loss and for potassium imbalance in the endolymph.

Adrenalectomy↗
PubMedDate not supplied

Gentamicin tympanoclysis: effects on the vestibular secretory cells.

Gentamicin application to the middle ear may relieve Meniere's disease, presumably by reducing endolymph secretion by the dark cells. To explore this possibility, the ears of adult cats were treated with daily intratympanic infusions of gentamicin until ataxia occurred. The temporal bones of these cats were then examined using electron microscopy. A 3 per cent solution of gentamicin resulted in ataxia after four treatments. Acute dark cell damage to basal infoldings seen after one month persisted at six months. Treatment with a 0.3 per cent solution required 15 and 21 days to effect ataxia and resulted in a similar damage pattern. Treatment with the 0.3 per cent solution for 13 days (i.e., before ataxia developed) resulted in subtle early lesions in the basal infoldings. Such lesions might affect the rate of endolymph secretion.

Animals↗
PubMedDate not supplied

Transepithelial cation movements in gerbil utricles.

The inner ear epithelium secretes potassium (K+) and absorbs sodium (Na+). The authors' experiments utilized, for the first time, isolation of the nonsensory from the sensory regions of the utricle in the vestibular labyrinth of the gerbil by means of injecting insulating seals. It was found that the isolated nonsensory region accumulated rubidium (Rb+) (as a marker for K+) in the endolymph to a level of eight times (41 mmol/l) that in the incubation medium (5 mmol/l) over a 90-minute period. However, Na+ rose during this period, suggesting that cells excluded from this preparation (sensory regions) may be involved in Na+ reabsorption. Further observations of the time course of changes in the luminal concentrations of cations suggested that the endpoints observed at 90 minutes represented a new steady state in which both Na+ and K+ concentrations were higher and lower, respectively, than under control conditions (by about 40 mmol/l each), but they were still each displaced from electrochemical equilibrium. This implies that the processes of Na+ absorption and/or K+ secretion may be shared in some way between the two regions. This finding is unexpected, based on previous models of endolymph production, in which ionic regulation has been assigned to nonsensory regions alone.

Animals↗
PubMed2001

Effects of acute and chronic hypertension on the labyrinthine barriers in rat.

Hearing loss, vertigo, and tinnitus have been related to arterial hypertension. The aim of the present work was to study the permeability of the blood-perilymph and of the labyrinthine barrier, between endolymph and perilymph, to small molecules during chronic and acute hypertension. Experiments were performed in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Acute hypertension was induced by phenylephrine. Perilymph was sampled from the first turn of the scala vestibuli and the Na, K, urea, and radioactive concentrations ((14)C-urea and (3)H-mannitol) were measured. In another experimental set, the endocochlear potential was recorded from the basal turn of scala media, before and after phenylephrine injection. The composition of the perilymph and the kinetic constants for (14)C-urea and (3)H-mannitol were similar in WKY and SHR, and not modified after acute hypertension. In endolymph, the endocochlear potential in SHR (+80+/-2.7 mV, n=24) was lower (P<0.001) than in WKY (+98+/-1.5 mV, n=29). The endocochlear potential was decreased by 40 mV during acute hypertensive peak in seven out of 19 WKY but not in SHR rats (n=13). In conclusion, chronic or acute hypertension did not severely alter the permeability to small molecules of the blood-perilymph barrier. The relationship between the low endocochlear potential and hypertension in SHR remains to be evaluated. After acute hypertensive peak, the presence of vascular protective mechanisms in the cochlea could account for the stable endocochlear potential recorded in SHR and 60% of normotensive rats.

Acute Disease↗
PubMed2002

Na+,K+-ATPase activity and ultrastructural localization in the tegmentum vasculosum in the cochlea of the duckling.

The tegmentum vasculosum of the avian cochlear duct mimics the stria vascularis of the mammalian cochlear duct in both location and structure, and previous studies indicate that it may be its functional counterpart with regard to endolymph synthesis. In the present study, we report on the enzymatic activity and ultrastructural localization of the Na+,K+-ATPase in the tegmentum vasculosum of the duckling. Na+,K+-ATPase activity was determined by measuring K+-dependent, ouabain-sensitive p-nitrophenyl phosphatase (p-NPPase) activity in homogenates of dissected regions of the cochlear duct. The ultrastructural localization of the Na+,K+-ATPase was identified using K+-dependent, ouabain-sensitive, p-NPPase cytochemistry. Specific enzyme activity was localized primarily in homogenates of the tegmentum vasculosum (2.27 micromol p-nitrophenyl phosphate/mg protein/min) when compared to homogenates of the entire cochlear duct (0.69 micromol p-nitrophenyl phosphate/mg protein/min). Reaction product for p-NPPase was localized primarily along the basolateral plasma membrane folds of the dark cells. The cytochemical deposits appeared to be located exclusively on the cytoplasmic side of the plasma membrane. The light cells were devoid of reaction product. Biochemical and cytochemical localization of p-NPPase activity on the basolateral plasma membrane folds of the dark cells of the tegmentum vasculosum in conjunction with the ultrastructural morphology of these cells is compatible with a Na+,K+-ATPase-dependent ion transport function related to endolymph synthesis.

4-Nitrophenylphosphatase↗
PubMed1997

Localization of pH regulating proteins H+ATPase and Cl-/HCO3- exchanger in the guinea pig inner ear.

Mechanisms that regulate endolymphatic pH are unknown. It has long been recognized that, because of the large positive endolymphatic potential in the cochlea, a passive movement of protons would be directed out of endolymph leading to endolymphatic alkalization. However, endolymphatic pH is close to that of blood, suggesting that H+ is being secreted into endolymph. Since the kidney and the inner ear are both actively engaged in fluid and electrolyte regulation, we attempted to determine whether proteins responsible for acid secretion in the kidney also exist in the guinea pig inner ear. To that end, a monoclonal antibody against a 31 kDa subunit of a vacuolar vH+ATPase and a polyclonal, affinity purified antibody against the AE2 Cl-/HCO3- exchanger (which can also recognize AE1 under some conditions) were used. In the cochlea, the strongest immunoreactivity for the vH+ATPase was found in apical plasma membranes and apical cytoplasm of strial marginal cells. These cells were negative for the Cl-/HCO3- exchanger. Certain cells of the inner ear demonstrated both apical staining for vH+ATPase and basolateral staining for the Cl-/HCO3- exchanger; these included interdental cells and epithelial cells of the endolymphatic sac. Cochlear cell types with diffuse cytoplasmic staining for vH+ATPase and a basolaterally localized Cl-/HCO3- exchanger included inner hair cells, root cells and a subset of supporting cells in the organ of Corti. Hair cells of the utricle, saccule and cristae ampullaris also expressed both vH+ATPase and the Cl-/HCO3- exchanger, but immunostaining for the vH+ATPase was less intense and less polarized than in the cochlea. These immunocytochemical results support a role for the vH+ATPase and Cl-/HCO3- exchanger in the regulation of endolymphatic pH and suggest that certain cells (including strial marginal cells and epithelial cells of the endolymphatic sac) may be specialized for this regulation.

Animals↗
PubMed1998

Evidence for a medial K+ recycling pathway from inner hair cells.

K+ effluxed from outer hair cells and their nerves is thought to flow laterally to strial marginal cells for recycling into scala media. Observations reported here provide evidence that K+ effluxed from inner hair cells and inner radial nerves travels medially through border cells, inner sulcus cells (ISCs), limbal fibrocytes and interdental cells (IDCs) for return to endolymph. Morphologic features of ISCs in the medial route resembled those of Hensen and Claudius cells in the lateral indicating an ion transport role for ISCs like that of Hensen and Claudius cells. Na,K-ATPase in plasmalemma of IDCs testified to their capacity to resorb and transport K+ through their known gap junctions. IDCs were differentiated into three subgroups. The most lateral IDCs formed short and long columns. Long columns contacted the medialmost ISC inferiorly and the undersurface of the tectorial membrane superiorly providing thereby a potential transcellular route for K+ transit from ISCs to endolymph. Short columns faced inner sulcus below and tectorial membrane above and accordingly possessed cells with opposite polarity at the bottom and top of the column. Short columns thus appeared situated to resorb electrolytes from limbal stroma for release into inner sulcus and beneath tectorial membrane at opposite ends of the column. The central IDCs were positioned for resorbing and transporting K+ effluxing from the Na,K-ATPase-rich stellate fibrocytes which spread toward the IDCs from near the inner sulcus. The most medial IDCs lined cuplike invaginations near the attachment of Reissner's membrane and lay apposed to light fibrocytes located between supralimbal fibrocytes and the medial IDCs. Content of Na,K-ATPase and position in the K+ transport route likened the limbal stellate fibrocytes to the spiral ligament type II fibrocytes and supralimbal fibrocytes to suprastrial fibrocytes in the lateral wall. From content of creatine kinase and position in the transport path, limbal light fibrocytes appeared analogous to spiral ligament type I fibrocytes. The additional finding that limbal fibrocytes showed unchanged or upregulated Na,K-ATPase immunoreactivity in aged gerbils with strial atrophy provided further evidence for an independent medial transport route and for the survival of inner hair cells in presbyacusis.

Aging↗
PubMed1999

Signs of endolymphatic hydrops after perilymphatic perfusion of the guinea pig cochlea with cholera toxin; a pharmacological model of acute endolymphatic hydrops.

There are indications that endolymph homeostasis is controlled by intracellular cAMP levels in cells surrounding the scala media. Cholera toxin is a potent stimulator of adenylate cyclase, i.e. it increases cAMP levels. We hypothesized that perilymphatic perfusion of cholera toxin might increase endolymph volume by stimulating adenylate cyclase activity, providing us with a pharmacological model of acute endolymphatic hydrops (EH). Guinea pig cochleas were perfused with artificial perilymph (15 min), with or without cholera toxin (10 microg/ml). The endocochlear potential (EP) was measured during and after perfusion. The summating potential (SP), evoked by 2, 4 and 8 kHz tone bursts, was measured via an apically placed electrode 0, 1, 2, 3 and 4 h after perfusion. Thereafter, the cochleas were fixed to enable measurement of the length of Reissner's membrane, reflecting EH. After perfusion the EP increased significantly over time in the cholera toxin group as compared to the controls. Also, the SP increased gradually at all frequencies in the cholera toxin group. Comparison within animals showed that the increase in SP became significant after 2 h at 4 kHz, after 3 h at 2 kHz and after 4 h at 8 kHz. In the control group the SP did not change significantly. The compound action potential (CAP) amplitude decreased monotonically over time at all frequencies in both the cholera toxin group and the control group, but it decreased faster in the cholera toxin group. Also, the cochlear microphonics amplitude decreased over time at all frequencies in both groups, but the decrease was significant only in the cholera toxin group after 3 h at 2 and 4 kHz. Quantification of the length of Reissner's membrane showed a small but insignificant enlargement in the cholera toxin treated animals compared to controls. These results are in accord with our view that EH is accompanied by an increase in SP and a decrease in CAP. Our results partially confirm previous results of Feldman and Brusilow (Proc. Natl. Acad. Sci. USA (1973) 73, 1761-1764). New aspects in relation to that study are the significantly increased EP and SP. In the classical EH model, based on obstruction of the absorptive function of the endolymphatic sac, increased SPs are accompanied by decreased EPs. In this cholera toxin model of EH, it is unlikely that the endolymphatic sac is involved. Apparently, EH can be based on mechanisms located in the cochlea itself as opposed to mechanisms located in the endolymphatic sac.

Animals↗
PubMed1984

Effects of glycerol on the inner ear fluid electrolytes of guinea pigs--oral and intravenous administration.

Under sodium pentobarbital anesthesia (25-35 mg/kg), serum, CSF and inner ear fluids from scala tympani perilymph, scala vestibuli perilymph, and scala media endolymph were collected from normal guinea pigs after the oral administration of glycerol (50%, 12 ml/kg) or the intravenous injection of glycerol (1.0 ml/kg). The sodium and potassium concentrations were assessed by microflame photometry. The electrolyte dynamics of the inner ear fluids were compared after these two routes of administration. Serum: There was no significant change in Na or K levels after either route of administration. CSF: The Na concentration increased rapidly after both intravenous and oral administrations of glycerol and remained high until the end of the experiment. The K concentration did not change significantly after intravenous injection. Scala tympani perilymph: The Na concentration increased transiently, after intravenous glycerol, while after oral administration it increased slowly and steadily. The K concentration increased only after oral administration. Scala vestibuli perilymph: The Na level increased slowly and steadily only after oral administration of glycerol, and the K level increased slightly after intravenous injection. Scala media endolymph: No changes in the K level occurred after either route of administration. After oral administration the Na level increased. These experiments show that dehydration persists longer after oral than after intravenous administration of glycerol. In the diagnosis of Meniere's disease, oral administration of glycerol is more effective than intravenous injection.

Administration, Oral↗
PubMed1975

The utriculo-endolymphatic valve: its functional significance.

A study was made of the anatomical structure and functional significance of the ultriculo-endolymphatic (UE) valve in man. The material consists of 170 human temporal bones of which 75 were chosen to show normal structure through nine decades of life, 29 with endolymphatic hydrops, 22 with developmental defects and 44 with pertinent staining characteristics of the endolymphatic fluid. The studies show that the UE valve is ideally suited to preserve the humoral and anatomical features of the pars superior (utricle and canals) from the developmental, disease, and traumatic susceptibilities of the pars inferior (cochlear duct and saccule). Its function probably is to permit the occasional egress of excessive accumulation of endolymph to be processed in the endolymphatic sac and to accomplish this while preserving the normal endolymph volume and membrane anatomy of the utricle and canals.

Adolescent↗
PubMed2006

Rupture of Reissner's membrane during acute endolymphatic hydrops in the guinea pig: a model for Ménière's disease?

CONCLUSION: The changes in cochlear function during a destructive acute endolymphatic hydrops were relatively small. This might be consistent with the hypothesis that an endolymphatic hydrops is a marker of disordered inner ear homeostasis rather than the cause of the clinical symptoms of Ménière's disease. OBJECTIVE: Assessment of cochlear function during induction of a destructive acute endolymphatic hydrops. MATERIALS AND METHODS: During repetitive microinjections of 0.5 microl of artificial endolymph at a rate of 50 nl/s the 2f1-f2 and f2-f1 cochlear microphonics distortion products (CMDP) and 2f1-f2 distortion products otoacoustic emissions (DPOAE) were recorded in the guinea pig. RESULTS: A 'catastrophe' occurred in the inner ear when 2.5-3.5 microl of artificial endolymph was injected. A rupture of Reissner's membrane was then found, most often in the apical turn of the cochlea. This rupture had only minor effects on the endocochlear potential, whereas it caused a marked decrease in 2f1-f2 DPOAE amplitude. The 2f1-f2 and f2-f1 CMDP amplitude increased during each injection prior to the rupture. After the rupture the f2-f1 CMDP amplitude decreased during each injection, possibly due to a shift of the cochlear transducer operating point position.

Animals↗
PubMed1993

N-ethylmaleimide-inhibited electrogenic K+ secretion in the ampulla of the frog semicircular canal.

1. The mechanisms of K+ secretion into endolymph were studied on a preparation of isolated semicircular canal with different pharmacological inhibitors. Three periods of 5 or 30 min were performed, the first as control, the second in the presence of the drugs added to the apical or the basolateral bathing solution, and the third as recovery. Apical fluid was sampled at the beginning and the end of each period, transepithelial potential was recorded, Na+, K+, and Cl- concentrations, and K+ efflux, with 86Rb+ as a tracer, were measured and K+ fluxes were calculated. 2. When both sides of the epithelium were bathed with perilymph-like solution, the epithelium absorbed Na+, secreted K+, and generated a lumen positive potential. 3. The ATPases inhibitors, ouabain (10(-5) and 10(-3) M) and N-ethylmaleimide (10(-4) and 10(-3) M) inhibited the electrogenic K+ secretion when added to the basolateral fluid. N-ethylmaleimide (10(-3) M) applied to the apical fluid during a 5 min period decreased the K+ influx by 43% and the transepithelial potential by 66%. Other ATPase inhibitors, harmaline (10(-3) M), omeprazole (10(-4) M), vanadate (10(-4) M and 10(-3) M), N,N'-dicyclohexylcarbodiimide (DCC, 10(-5) M), 7-chloro-4-nitrobenz-2-oxa-1,3-diazole (NBD-Cl, 5 x 10(-6) M and 5 x 10(-5) M), and bafilomycin (10(-7) M) did not affect the K+ transport nor the transepithelial potential when they were added to the apical fluid. 4. The Na(+)-K(+)-Cl- co-transporter inhibitor, bumetanide, decreased both the transepithelial potential and the K+ transport when added to the basolateral solution but not to the apical one. At 10(-6) M, bumetanide maximally decreased the K+ influx by about 60%. 5. K+ channel blockers, quinine (10(-4) M), TEA (5 x 10(-3) M), added to the apical solution and barium (2 x 10(-3) M) added to either the apical or the basolateral solutions, did not affect the K+ transport and the transepithelial potential. 6. The carbonic anhydrase inhibitor acetazolamide (10(-3) M) added to both apical and basolateral solutions did not affect the K+ transport and the transepithelial potential. 7. It is concluded that, in the ampulla of the semicircular canal, a basolateral Na(+)-K(+)-Cl- co-transporter energized by the Na+, K(+)-ATPase was involved for 60% in the K+ secretion into endolymph. The electrogenic K+ transport would partly depend on a N-ethylmaleimide-sensitive protein possibly located at the apical plasma membrane or intracellularly.

Animals↗
PubMed1967

Cochlear function and sodium and potassium activated adenosine triphosphatase.

The maintenance of the cation gradients between endolymph and perilymph in the cochlea requires the operation of a cation pump. An adenosine triphosphatase system activated by sodium and potassium is present in high activity in the cochlear membranes (tegmentum vasculosum and stria vascularis). The cochlear microphonic potential is inhibited by perilymphatic perfusion of ouabain and erythrophleine. Since the microphonic potential depends on the high concentration of potassium ions in the endolymph, our findings strongly suggest the operation of an adenosine triphosphatase cation pump system activated by sodium and potassium, in the generation of cochlear cation gradients.

Animals↗
PubMed2001

Location and function of the epithelial Na channel in the cochlea.

In the cochlea, endolymph is a K-rich and Na-poor fluid. The purpose of the present study was to check the presence and to assess the role of epithelial Na channel (ENaC) in this organ. alpha-, beta-, and gamma-ENaC subunit mRNA, and proteins were detected in rat cochlea by RT-PCR and Western blot. alpha-ENaC subunit mRNA was localized by in situ hybridization in both epithelial (stria vascularis, spiral prominence, spiral limbus) and nonepithelial structures (spiral ligament, spiral ganglion). The alpha-ENaC-positive tissues were also positive for beta-subunit mRNA (except spiral ganglion) or for gamma-subunit mRNA (spiral limbus, spiral ligament, and spiral ganglion), but the signals of beta- and gamma-subunits were weaker than those observed for alpha-subunit. In vivo, the endocochlear potential was recorded in guinea pigs under normoxic and hypoxic conditions after endolymphatic perfusion of ENaC inhibitors (amiloride, benzamil) dissolved either in K-rich or Na-rich solutions. ENaC inhibitors altered the endocochlear potential when Na-rich but not when K-rich solutions were perfused. In conclusion, ENaC subunits are expressed in epithelial and nonepithelial cochlear structures. One of its functions is probably to maintain the low concentration of Na in endolymph.

Action Potentials↗
PubMed1994

Sensory transduction of head velocity and acceleration in the toadfish horizontal semicircular canal.

1. Sinusoidal mechanical indentation of the long-and-slender limb of the horizontal semicircular canal and/or utricle was used to produce adequate stimulation of the labyrinth. Indentation of the canal increased, while indentation of the utricle decreased the afferent discharge rate. This follows because indentation of the canal and utricle produce oppositely directed mechanical stimuli as defined by endolymph flow, transcupular pressure, and cupular deflection. Simultaneous in-phase indentations of both the canal and utricle, with amplitudes adjusted to produce equal (but opposite) magnitudes of afferent response modulation, generate destructive interaction that minimizes the afferent modulation, whereas sinusoidal indentation 180 degrees out-of-phase generates constructive interaction that maximizes the afferent modulation. This observation correlates directly with analysis of the labyrinthine elasto-hydrodynamics which predicts that balanced in-phase indentations minimize macromechanical endolymph flow through the ampullary cross section and maximize the dilatational pressure within the ampulla acting equally on both sides of the cupula and across the labyrinthine wall. 2. Two groups of afferents are identified according to their response to balanced sinusoidal indentation of the canal limb and the utricle. In one group there is complete destructive interaction and the afferent response can be effectively nulled by adjusting the relative amplitude and phase of the two stimuli. In the second group a residual afferent response remains that cannot be nulled. The residual is described in the model as unit-specific sensitivity to dilatational pressure acting equally on both sides of the cupula.

Afferent Pathways↗