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The effects of a superior-semicircular-canal (SSC) dehiscence (SSCD) on hearing sensitivity via the air-conduction (AC) and bone-conduction (BC) pathways were investigated using a three-dimensional finite-element (FE) model of a human middle ear coupled to the inner ear. Dehiscences were modeled by removing a section of the outer bony wall of the SSC and applying a zero-pressure condition to the fluid surface thus exposed. At each frequency, the basilar-membrane velocity, vBM, was separately calculated for AC and BC stimulation, under both pre- and post-dehiscence conditions. Hearing loss was calculated as the difference in the maximum magnitudes of vBM between the pre- and post-dehiscence conditions representing a change in hearing threshold. In this study, BC excitations were simulated by applying rigid-body vibrations to the model along the directions of the (arbitrarily defined) x, y, and z axes of the model. Simulation results are consistent with previous clinical measurements on patients with an SSCD and with results from earlier lumped-element electrical-circuit modeling studies, with the dehiscence decreasing the hearing threshold (i.e., increasing vBM) by about 35 dB for BC excitation at low frequencies, while for AC excitation the dehiscence increases the hearing threshold (i.e., decreases vBM) by about 15 dB. A new finding from this study is that the initial width (defined as the width of the edge of the dehiscence where the flow of the fluid-motion wave from the oval window meets it for the first time) on the vestibular side of the dehiscence has more of an effect on vBM than the area of the dehiscence. Analyses of dehiscence effects using the FE model further predict that changing the direction of the BC excitation should have an effect on vBM, with vBM being about 20 dB lower due to BC excitation parallel to the longitudinal direction of the BM in the hook region (the x direction) as compared to excitations in other directions (y and z). BC excitation in the x direction and with a 'center' dehiscence located midway along the length of the SSC causes a reduction in the anti-symmetric component of the fluid pressure across the BM, as compared to the other directions of BC excitation, which results in a decrease in vBM at high frequencies. This article is part of a special issue entitled "MEMRO 2012"., (Copyright © 2013. Published by Elsevier B.V.)

We have used sinusoidal and band-limited Gaussian noise stimuli along with information measures to characterize the linear and non-linear responses of morpho-physiologically identified posterior canal (PC) afferents and to examine the relationship between mutual information rate and other physiological parameters. Our major findings are: 1) spike generation in most PC afferents is effectively a stochastic renewal process, and spontaneous discharges are fully characterized by their first order statistics; 2) a regular discharge, as measured by normalized coefficient of variation (cv*), reduces intrinsic noise in afferent discharges at frequencies below the mean firing rate; 3) coherence and mutual information rates, calculated from responses to band-limited Gaussian noise, are jointly determined by gain and intrinsic noise (discharge regularity), the two major determinants of signal to noise ratio in the afferent response; 4) measures of optimal non-linear encoding were only moderately greater than optimal linear encoding, indicating that linear stimulus encoding is limited primarily by internal noise rather than by non-linearities; and 5) a leaky integrate and fire model reproduces these results and supports the suggestion that the combination of high discharge regularity and high discharge rates serves to extend the linear encoding range of afferents to higher frequencies. These results provide a framework for future assessments of afferent encoding of signals generated during natural head movements and for comparison with coding strategies used by other sensory systems. This article is part of a Special Issue entitled: Neural Coding., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Na(+) concentrations in endolymph must be controlled to maintain hair cell function since the transduction channels of hair cells are cation-permeable, but not K(+)-selective. Flooding or fluctuations of the hair cell cytosol with Na(+) would be expected to lead to cellular dysfunction, hearing loss and vertigo. This review briefly describes cellular mechanisms known to be responsible for Na(+) homeostasis in each compartment of the inner ear, including the cochlea, saccule, semicircular canals and endolymphatic sac. The influx of Na(+) into endolymph of each of the organs is likely via passive diffusion, but these pathways have not yet been identified or characterized. Na(+) absorption is controlled by gate-keeper channels in the apical (endolymphatic) membrane of the transporting cells. Highly Na(+)-selective epithelial sodium channels (ENaCs) control absorption by Reissner's membrane, saccular extramacular epithelium, semicircular canal duct epithelium and endolymphatic sac. ENaC activity is controlled by a number of signal pathways, but most notably by genomic regulation of channel numbers in the membrane via glucocorticoid signaling. Non-selective cation channels in the apical membrane of outer sulcus epithelial cells and vestibular transitional cells mediate Na(+) and parasensory K(+) absorption. The K(+)-mediated transduction current in hair cells is also accompanied by a Na(+) flux since the transduction channels are non-selective cation channels. Cation absorption by all of these cells is regulated by extracellular ATP via apical non-selective cation channels (P2X receptors). The heterogeneous population of epithelial cells in the endolymphatic sac is thought to have multiple absorptive pathways for Na(+) with regulatory pathways that include glucocorticoids and purinergic agonists., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Multiunit activity during horizontal sinusoidal motion was recorded from pairs of oculomotor, trochlear, or abducens nerves of an in vitro turtle brainstem preparation that received inputs from intact semicircular canals. Responses of left oculomotor, right trochlear and right abducens nerves were approximately aligned with leftward head velocity, and that of the respective contralateral nerves were in-phase with rightward velocity. We examined the effect of sectioning or injecting lidocaine (1-2 microL of 0.5%) into the right vestibular nerve. Nerve block caused a striking phase shift in the evoked response of right oculomotor and left trochlear nerves, in which (rightward) control responses were replaced by a smaller-amplitude response to leftward table motion. Such "phase-reversed" responses were poorly defined in abducens nerve recordings. Frequency analysis demonstrated that this activity was advanced in phase relative to post-block responses of the respective contralateral nerves, which were in turn phase-advanced relative to pre-block controls. Phase differences were largest (approximately 10 degrees) at low frequencies (approximately 0.1 Hz) and statistically absent at 1 Hz. The phase-reversed responses were further investigated by eliminating individual canal input from the left labyrinth following right nVIII block, which indicated that the activation of the vertical canal afferents is the source of this activity.

The orientations of the semicircular canals determines the response of the canals to head rotations and, in turn, the brain's ability to interpret those motions. The geometry of chinchillas' semicircular canals has never been reported. Volumetric representations of three chinchilla skulls were generated using a microCT scanner. The centroids of each semicircular canal lumen were identified as they passed through the image slices and were regressed to a plane. Unit vectors normal to the plane representing canal orientations were used to calculate angles between canal pairs. Pitch and roll maneuvers required to bring any canal into the horizontal plane for physiologic investigation were calculated. The semicircular canals of the chinchilla were found to be relatively planar. The horizontal canal was found to be oriented 55.0 degrees anteriorly upward. Pairs of ipsilateral chinchilla canals were not orthogonal and contralateral synergistic pairs were not parallel. Despite this arrangement, the canal plane unit normal vectors were organized to respond with approximately equal overall sensitivity to rotations in any direction. The non-orthogonal chinchilla labyrinth may provide an opportunity to determine whether the frame of reference used by the central vestibular and oculomotor system is based on directions of afferent maximum sensitivity or prime directions.

Although the effectiveness of histamine-related drugs in the treatment of peripheral and central vestibular disorders may be explained by their action on the vestibular nuclei, it has also been shown that antivertigo effects can take place at the peripheral level. In this work, we examined the actions of H3 histaminergic agonists and antagonists on the afferent neuron electrical discharge in the isolated inner ear of the axolotl. Our results indicate that H3 antagonists such as thioperamide, clobenpropit, and betahistine (BH) decreased the electrical discharge of afferent neurons by interfering with the postsynaptic response to excitatory amino acid agonists. These results lend further support to the idea that the antivertigo action of histamine-related drugs may be caused, at least in part, by a decrease in the sensory input from the vestibular endorgans. The present data show that the inhibitory action of the afferent neurons discharge previously described for BH is not restricted to this molecule but is also shared by other H3 antagonists.

The low voltage gain in type I hair cells implies that neurotransmitter release at their afferent synapse should be mediated by low voltage activated calcium channels, or that some peculiar mechanism should be operating in this synapse. With the patch clamp technique, we studied the characteristics of the Ca(2+) current in type I hair cells enzymatically dissociated from rat semicircular canal crista ampullaris. Calcium current in type I hair cells exhibited a slow inactivation (during 2-s depolarizing steps), was sensitive to nimodipine and was blocked by Cd(2+) and Ni(2+). This current was activated at potentials above -60 mV, had a mean half maximal activation of -36 mV, and exhibited no steady-state inactivation at holding potentials between -100 and -60 mV. This data led us to conclude that hair cell Ca(2+) current is most likely of the L type. Thus, other mechanisms participating in neurotransmitter release such as K(+) accumulation in the synaptic cleft, modulation of K(+) currents by nitric oxide, participation of a Na(+) current and possible metabotropic cascades activated by depolarization should be considered.

The horizontal and vertical vestibulo ocular reflex (VOR) of head tilted (het) mutant mice was compared to C57BL/6 controls. Eye movements were recorded in darkness using a temporarily attached search coil. Contributions of semicircular canal versus otolith organ signals were investigated by providing a canal only (vertical axis) or canal plus otolith organ (horizontal axis) stimulus. In controls, rotations that stimulated only the canals (upright yaw and on tail roll) produced accurate VOR timing during middle frequency rotations at 0.5 Hz (gain 0.27, phase error 6 degrees), and a phase advanced VOR during low frequency rotations at 0.05 Hz (0.05, 115 degrees). In het mutant mice, these rotations produced a highly attenuated VOR response and phase errors at both 0.5 Hz (0.11, 42 degrees) and 0.05 Hz (0.01, 36 degrees). In controls, rotations that stimulated both the otolith organs and semicircular canals (upright roll and on tail yaw) produced higher VOR gains overall than were elicited during vertical axis rotations, with phase accurate VOR at both 0.5 Hz (0.52, 4 degrees) and 0.05 Hz (0.34, 9 degrees). In het mutant mice, these rotations produced a highly attenuated VOR response and phase errors at both 0.5 Hz (0.14, 51 degrees) and 0.05 Hz (0.01, 43 degrees). During constant velocity rotations about an earth horizontal axis, eye velocity bias and modulation were virtually absent in het mutant mice, while robust in controls. Control mice produced compensatory ocular deviations in response to static head tilt, but responses in het mice were weak and inconsistent. These results show that het mice not only lack all aspects of otolith mediated VOR, but also are deficient in canal mediated VOR. Because semicircular canals are normal in het mice, we conclude that central neurons of the canal VOR are dependent on otolith organ signals for normal performance.

We studied hair cell regeneration in the crista ampullaris of the lizard Podarcis sicula both in untreated animals and at early and late time intervals following a single high dose of gentamicin. The study was carried out using the S-phase marker 5-bromo-2'-deoxyuridine. Our ultrastructural and immunofluorescence studies showed that both apoptosis and hair cell regeneration happen in the lizard crista ampullaris in untreated animals, and that regenerative processes are greatly accelerated after treatment with the aminoglycoside antibiotic gentamicin. Our observations indicate that hair cell regeneration is strongly implicated in the repair of damaged sensory epithelium, and that new hair cells appear likely to arise from supporting cells.

The response of the semicircular canal (SCC) to the group I mGluR-selective agonist dihydroxyphenylglycine (DHPG; 300 microM) - facilitation of afferent discharge rate - was dose-dependently reduced by the phospholipase C inhibitor U-73122 (1-100 microM; IC(50): 22 microM), the smooth endoplasmic reticulum Ca(++) ATPase inhibitor thapsigargin (100 nM-3 microM; IC(50): 500 nM), and xestospongin C (100 pM-1 microM; IC(50): 11 nM), an inositol trisphosphate receptor (IP(3)R) antagonist. Ryanodine, a modulator of Ca(++)-induced Ca(++) release, biphasically facilitated, then suppressed this response (1 nM-1 mM; approximate IC(50): 50 microM). 5 mM caffeine increased the amplitude (34.6+/-13.4%) and duration (453+/-169.8%; n=4) of the response of the SCC to DHPG, while 50 mM caffeine eliminated this response (n=2). The protein kinase C inhibitor bisindolylmaleimide I-HCl (10-100 microM; n=3) and the cyclic-ADP ribose antagonist 8-Br-cyclic-ADP ribose (1-10 microM; n=3) had no effect on the response of the SCC to DHPG. These data suggest that the increase in transmitter release following activation of group I mGluRs on vestibular hair cells is associated with intracellular Ca(++) release from both IP(3)-sensitive and ryanodine/caffeine-sensitive intracellular Ca(++) stores. Such positive feedback on transmitter release may serve to enhance the contrast between the spontaneous and stimulus-evoked modes of hair cell transmitter release, thereby optimizing signal discrimination at the synapse between hair cells and vestibular afferent fibers.

Vestibular evoked potentials during rotation of human subjects around their naso-occipital roll-axis were recorded. The effect of stimulating the vertical semicircular canals and otolithic stimulation was investigated by comparing the evoked potentials obtained under the 1-G condition with those recorded in microgravity conditions. Subjects lay on their side with the head in the center of rotation and were tilted feet upward (roll up) and back into the lying position (roll down). The microgravity environment was created by parabolic flight maneuvers. In microgravity, transient bell-shaped negativity was recorded for roll up and down motion. In the 1-G condition the potentials were superimposed on sustained components, probably due to additional otolithic stimulation. It seems to be possible to separate the evoked responses in a transient canal response and a sustained otolithic response. The results are encouraging with respect to the goal of developing a tool for the selective assessment of canal and otolithic responses of the vestibular system., (Copyright 2002 Elsevier Science B.V.)

Vestibular nerve branches innervating the sensory epithelia of the three semicircular canals or of the three otolith organs of frogs were selectively labeled in-vitro with biocytin. Labeled afferent fibers from the semicircular canals, utricle, and lagena were encountered in each of the four vestibular nuclei and their projections overlapped considerably. Saccular afferent fibers projected to the dorsal (acoustic) nuclei and smaller projections to the vestibular nuclei were regionally restricted. Per semicircular canal or otolith organ about equal numbers (11-14) of medium sized vestibular neurons (between 7.5 and 17 microm in diameter) were dye-coupled to afferent fibers. Most of these dye-coupled vestibular neurons were located in the lateral and descending vestibular nuclei between the VIIIth and IXth nerves. The superior vestibular nucleus was relatively free of dye-coupled vestibular neurons. The location of this subpopulation of central vestibular neurons supports the notion that these neurons are part of a particular vestibulospinal pathway. In addition, from each of the canal and/or otolith organs about 3-4 efferent vestibular neurons were labeled retrogradely. These neurons (between 15 and 26 microm in diameter) were located ventral to the vestibular nuclear complex. The branching of efferent vestibular neurons was shown by the presence of neurons that were double labeled by two different fluorescent dyes applied in the same experiment to the anterior and posterior ramus of the same VIIIth nerve, respectively. The branching of these efferent neuron axons explained the presence of collaterals and terminals in the sensory epithelia of a number of untreated ipsilateral endorgans.

A microthermistor positioned close to the exposed posterior semicircular canal in isolated labyrinth preparations of the frog was used to stimulate the sensory organ. Our results indicated that, depending on the position of the heater, the induced endolymphatic convection currents may result in either excitatory or inhibitory cupular deflections and thus in a modulation of ampullar receptor resting activity. Other possible thermal-dependent mechanisms, such as a direct action of the stimulus on vestibular sensors or endolymphatic volume changes, had, in the present experimental conditions, a minor role. Caloric stimulation could therefore represent a novel method to stimulate the semicircular canals 'in situ'.

Cationic polyethyleneimine (PEI) administered intravenously was transported to anionic sites on the capillary and subepithelial basal laminae (BL) in the vestibular labyrinth. Therefore, changes in the PEI distribution on the BL reflect changes in the transport system in the vestibular labyrinth. A 0.1% PEI solution was administered intravenously (7.5 ml/kg) to developing (1, 4, 7, 14 days after birth) and adult rats in order to investigate the development of the macromolecular transport in the ampulla of the semicircular canal as a function of age. After 1 h, the bony labyrinth was removed and embedded in Epoxy resin. Ultrathin sections of the ampulla were then examined with a transmission electron microscope. In the subepithelial BL in the dark cell area and capillary BL in the crista ampullaris, the PEI distribution in both 1- and 4-day-old rats was markedly increased compared to that in either 7-, 14-day or adult rats. In the sensory cells in 1-, 4-day or 7-day-old rats, PEI density and area was significantly greater than in the adult rats. These findings suggest that the macromolecular transport system in the developing rat ampulla becomes mature by 14 days after birth and that the maturation of its transport system in the ampulla is strongly associated with that in the stria vascularis.

This research sought to test the presence and function of metabotropic excitatory amino acid receptors (mGluR) in the frog semicircular canal (SCC). The mGluR agonist +/- 1-aminocyclopentane-trans-1,3-dicarboxylate (ACPD) produced an increase in afferent firing rates of the ampullar nerve of the intact posterior canal. This increase was not due to a stimulation of cholinergic efferent terminals or the acetylcholine (ACh) receptor, since atropine, in concentrations which blocked the response to exogenous acetylcholine, did not affect the response to ACPD. Likewise, ACPD effects were not due to stimulation of postsynaptic NMDA receptors, since the NMDA antagonist D(-)-2-amino-5-phosphonopentanoate (AP-5) did not affect the response to ACPD, reinforcing the reported selectivity of ACPD for mGluRs. When the SCC was superfused with artificial perilymph known to inhibit hair cell transmitter release (i.e. low Ca-high Mg), ACPD failed to increase afferent firing. This suggests that the receptor activated by ACPD is located on the hair cell. Pharmacological evidence suggested that the mGluRs involved in afferent facilitation belong to Group I (i.e. subtypes 1 and 5). In fact, the Group III agonist AP-4 had no effect, and the ACPD facilitatory effect was blocked by the Group I mGluR antagonists (S)-4-carboxyphenylglycine (CPG) and (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA). Additional pharmacological evidence supported the presence of Group I mGluRs. Interestingly, the mGluR antagonists, AIDA and 4CPG, by themselves did not affect the resting firing rates of ampullar afferents. This may suggest that the mGluRs are not involved in resting activity but perhaps only in evoked activity (as suggested in Guth et al. (1991) Hear. Res. 56, 69-78). In addition, the mRNA for the mGluR1 has been detected in hair cells of both SCC, utricle, and saccule. In summary, the evidence points to an mGluR localized to the hair cell (i.e. an autoreceptor) which may be activated to produce a positive feedback augmentation of evoked but not resting transmitter release and thus affect afferent activity.

Previous studies have shown that galvanic stimulation of semicircular canal organs can modulate their afferent discharge. However, it has not been resolved whether this modulation derived from direct stimulation of hair cells, afferent nerve fibers, some combination of the two, or some as yet unknown path. This problem is addressed in the present study. Experiments were designed first to determine the gross current path necessary for the DC current to modulate afferent firing. These led to the conclusion that the current path had to flow between endolymph and perilymph across the neuroepithelium. Next, the various components in this established path were considered: the afferents, the hair cells, between the hair cells, or some combination of the three. These experiments led to the conclusion that the current pathway was across the hair cells causing transmitter release and thus affecting afferent activity.

The connections of a potential auditory circuit were determined in the medulla of the toadfish (Opsanus tau). Fluorescent dextran amines placed in the medial torus semicircularis (mTS) retrogradely filled cells primarily in the dorsal region of the descending octaval nuclei (DON) with contralateral predominance. Fluorescent dextran amines placed in the DON revealed commissural fibers that cross the midline with the internal arcuate tract. The interconnections are consistent with a dorsal-ventral organization of the DON: reciprocal innervation is present for the left and right dorsal zones of the DON and for the left and right ventral zones of the DON. Based on projections to the medial (auditory) TS and the reciprocal connections, the dorsal region of the DON appears to be the major auditory processing site in the medulla and also may be a site for directional, binaural comparisons. The ventral region of the DON may be a site for bilateral vestibular processing. Double-labelling experiments revealed that some of the descending octaval cells projecting to the contralateral DON also project to the mTS. Based on the auditory pathway indicated by this study, future neurophysiological investigations of sensitivity to directional sound stimuli should begin in the dorsal DON of the toadfish.

The effects of changes in perilymphatic tonicity on the semicircular canal were investigated by combining the measurements of transepithelial potential and endolymphatic ionic composition in the isolated frog posterior canal with the electrophysiological assessment of synaptic activity and sensory spike firing at the posterior canal in the isolated intact labyrinth. In the isolated posterior canal, the endolymph was replaced by an endolymph-like solution of known composition, in the presence of basolateral perilymph-like solutions of normal (230 mosmol/kg), reduced (105 mosmol/kg, low NaCl) or increased osmolality (550 mosmol/kg, Na-Gluconate added). Altered perilymphatic tonicity did not produce significant changes in endolymphatic ionic concentrations during up to 5 min. In the presence of hypotonic perilymph, decreased osmolality, K and Cl concentrations were observed at 10 min. In the presence of hypertonic perilymph, the endolymphatic osmolality began to increase at 5 min and by 10 min Na concentration had also significantly increased. On decreasing the tonicity of the external solution an immediate decline was observed in transepithelial potential, whereas hypertonicity produced the opposite effect. In the intact frog labyrinth, mEPSPs and spike potentials were recorded from single fibers of the posterior nerve in normal Ringer's (240 mosmol/kg) as well as in solutions with modified tonicity. Hypotonic solutions consistently decreased and hypertonic solutions consistently increased mEPSP and spike frequencies, independent of the species whose concentration was altered. These effects ensued within 1-2 min after the start of perfusion with the test solutions. In particular, when the tonicity was changed by varying Na concentration the mean mEPSP rate was directly related to osmolality. Size histograms of synaptic potentials were well described by single log-normal distribution functions under all experimental conditions. Hypotonic solutions (105 mosmol/kg) markedly shifted the histograms to the left. Hypertonic solutions (380-550 mosmol/kg, NaCl or Na-Gluconate added) shifted the histograms to the right. Hypertonic solutions obtained by adding sucrose to normal Ringer's solution (final osmolality 550 mosmol/kg) increased mEPSP and spike rates, but did not display appreciable effects on mEPSP size. All effects on spike discharge and on mEPSP rate and size were rapidly reversible. In Ca-free, 10 mM EGTA, Ringer's solution, the sensory discharge was completely abolished and did not recover on making the solution hypertonic. These results indicate that perilymphatic solutions with altered tonicity produce small and slowly ensuing changes in the transepithelial parameters which may indirectly affect the sensory discharge rate, whereas relevant, early and reversible effects occur at the cytoneural junction. In particular, the modulation of mEPSP amplitude appears to be postsynaptic; the presynaptic effect on mEPSP rate of occurrence is presumably linked to local calcium levels, in agreement with previous results indicating that calcium inflow is required to sustain basal transmitter release in this preparation.

Immunolabeling patterns of the immediate early gene-related protein Fos in the gerbil brainstem were studied following stimulation of the sacculus by both hypergravity and galvanic stimulation. Head-restrained, alert animals were exposed to a prolonged (1 h) inertial vector of 2 G (19.6 m/s2) head acceleration directed in a dorso-ventral head axis to maximally stimulate the sacculus. Fos-defined immunoreactivity was quantified, and the results compared to a control group. The hypergravity stimulus produced Fos immunolabeling in the dorsomedial cell column (dmcc) of the inferior olive independently of other subnuclei. Similar dmcc labeling was induced by a 30 min galvanic stimulus of up to -100 microA applied through a stimulating electrode placed unilaterally on the bony labyrinth overlying the posterior canal (PC). The pattern of vestibular afferent firing activity induced by this galvanic stimulus was quantified in anesthetized gerbils by simultaneously recording from Scarpa's ganglion. Only saccular and PC afferent neurons exhibited increases in average firing rates of 200-300%, suggesting a pattern of current spread involving only PC and saccular afferent neurons at this level of stimulation. These results suggest that alteration in saccular afferent firing rates are sufficient to induce Fos-defined genomic activation of the dmcc, and lend further evidence to the existence of a functional vestibulo-olivary-cerebellar pathway of adaptation to novel gravito-inertial environments.

The motor development after uni- or bilateral vestibular deprivation from the 5th or 16th postnatal day was studied in 23 rats between the 6th and the 60th day. Their motor behaviour was compared to that of 17 normal rats. Vestibular deprivation from the 5th day causes a marked retardation in motor development. Our results suggest that this retardation is caused by non-optimal stabilization of the trunk during development. Vestibular deprivation from the 16th day causes only short lasting disturbances of motor behaviour for one or two days. The main permanent effect of bilateral vestibular deprivation is head oscillation during locomotion. The temporal organization of the motor behaviour of rats bilaterally deprived from the 5th day was disturbed as well. These rats show more bouts of locomotion, rearing and pivoting.

We investigated, psychophysically, the influence of body rotation on visual motion direction thresholds for both upright sitting and tilted observers. Four angular accelerations (0, 20, 40 and 60 degrees/s2) were combined with 3 concurrent backward-tilt positions (0, 45 and 90 degrees). This led to combined stimulation of the semicircular canals and otoliths. Vestibular stimulation was combined with a visual motion stimulus. Random-dot kinematograms in which varying percentages of pixels coherently moving to the left were presented upon a background of otherwise randomly moving pixels (random walk). The smallest percentage of coherently moving pixels leading to a clear perception of motion direction represented as the perceptual threshold. Angular accelerations about the longitudinal body axis significantly increased motion-direction thresholds. Concurrent backward tilt did not influence thresholds. These results differ from those of studies in which translational linear acceleration was employed. Our results support the view that it is necessary to distinguish between linear acceleration caused by gravitational forces and that caused by additional linear accelerations about the x-, y-, and z-axes.

Responses of 35 Purkinje cells in decerebrate cats were recorded during 0.5 Hz rotations in 4-11 vertical planes and the horizontal plane to determine their semicircular canal input. Most neurons received convergent input from two canals (21 neurons) or 3 canals (5 neurons). Few Purkinje cells were maximally sensitive to rotations about an axis appropriate to their inferior olivary input as determined by Gerrits and Voogd [15,24,27,49].

Transepithelial voltage (Vt) and resistance (Rt) were measured across the dark cell epithelium of the gerbil ampulla using a micro Ussing chamber of improved design in order to test the view that the histologically similar epithelia in the utricle and in the ampullae exhibit similar electrophysiologic functions. Vt was found to be 8.0 +/- 0.3 mV and Rt was 11.6 +/- 0.4 ohm-cm2 (N = 179) when both sides of the tissue were perfused with symmetric perilymph-like solution. The equivalent short circuit current (Isc = Vt/Rt) was 712 +/- 18 microA/cm2 (N = 179). Isc was reduced from 638 +/- 60 to 48 +/- 16 microA/cm2 (N = 14) by basolateral perfusion of 10(-3) M ouabain and from 538 +/- 27 to 27 +/- 4 microA/cm2 (N = 15) by basolateral perfusion of 5 x 10(-5) M bumetanide. Basolateral K+ steps (Na+ substitution) from 3.6 to 25 mM increased Vt from 6.5 +/- 0.5 to 12.2 +/- 0.6 mV and reduced Rt from 9.7 +/- 0.7 to 7.4 +/- 0.5 ohm-cm2 (N = 43). Apical K+ steps from 3.6 to 25, to 100 mM or to 145 mM led to a decrease in both Vt and Rt. The steady state Vt during apical perfusion of 145 mM K+ was near zero. Upon return to 3.6 mM K+, Vt transiently overshot its original level. Apical Cl- steps from 150 to 50 mM (gluconate substitution) monophasically decreased Vt from 5.9 +/- 0.7 to 4.1 +/- 0.8 mV (N = 15) and increased Rt from 9.6 +/- 1.3 to 12.0 +/- 1.5 ohm-cm2 (N = 14).(ABSTRACT TRUNCATED AT 250 WORDS)

A hydraulically driven, digitally servo-controlled multi-axes rotary chair is described. This device generates motion profiles with the subjects head in the center of rotation mainly in order to adequately stimulate the semicircular canals which are sensitive sensors for angular accelerations. This newly developed apparatus allows for motion stimuli which are below the vestibular threshold up to accelerations of 12 rad/s2 (688 degrees/s2) and is thus suitable for a variety of experiments in the field of vestibular, oculomotor, and intersensory research in 3-dimensional space.

In the inner ear, calcium appears to play a major role in different processes including mechanoelectrical transduction, adaptation during prolonged stimulation and electrical resonance. The aim of the present study was to investigate the effect of an increase of the cytosolic calcium content and a reduction of the perilymphatic concentration of calcium, on the bioelectrical activity of the isolated frog semicircular canal. Under resting conditions, the spontaneous activity of the afferent fibers and the difference of potential between the endolymphatic and perilymphatic compartments, called endolymphatic potential, were recorded. When the sensory epithelium was mechanically stimulated three additional parameters were investigated: the variations of the endolymphatic potential (ampullar direct current), the variations of the ampullar nerve potential (nerve direct current) and the frequency of the evoked afferent spikes. Increase of the intracellular calcium concentration by administration of the calcium ionophore A23187 (3 x 10(-6) M, 20 min) into the perilymphatic compartment, caused a biphasic effect on the spontaneous activity of the ampullar nerve which increased rapidly, reaching a maximum within 15 min, and then gradually declined to stabilize at 74% of the control 1 h after withdrawal of A23187. A23187 did not induce any modifications of the endolymphatic potential, the ampullar direct current or the frequency of the evoked afferent spikes. In contrast, A23187 induced a significant reduction of the nerve direct current which decreased by 31% of the control 1 h after withdrawal of the ionophore. Gradual reduction of the perilymphatic concentration of calcium (from 2 to 1 mM) induced a dose-dependent increase of the spontaneous activity of the ampullar nerve and the frequency of the evoked afferent spikes. Reduction of the perilymphatic calcium concentration from 1.6 to 1.2 mM caused a transient increase of the endolymphatic potential, while 1 mM Ca2+ induced a decrease to 88% of the control. The nerve direct current slightly increased for calcium concentrations ranging from 1.8 to 1.4 mM and decreased in the presence of 1.2 mM CaCl2. These data suggest that an increase of calcium into the cytosol induces an alteration of the mechanisms responsible for the spontaneous release of the afferent neurotransmitter and the electrogenic spreading of the postsynaptic potentials. In contrast, an excess of calcium does not impair the mechanisms involved in the generation of the action potentials. Our results also suggest that reduction of the perilymphatic calcium concentration may lead to modifications of the physical and electrical properties of the cell membranes of the labyrinthine epithelium and/or the ampullar afferent fibers.

To investigate the neural substrate of vestibulo-sympathetic reflexes, we studied the responses of neurons in the rostral ventrolateral medulla (RVLM) of decerebrate cats to natural stimulation of the labyrinth in vertical and horizontal planes. The RVLM is a major source of excitatory inputs to sympathetic preganglionic neurons. The animals used in these studies were baroreceptor-denervated and vagotomized and had a cervical spinal transection so that inputs from tilt-sensitive receptors outside of the labyrinth did not influence the units we recorded. Of the 38 neurons whose type of vertical vestibular inputs could be classified, the majority (27) received signals mainly from otolith organs. Only 4 of the neurons received inputs predominantly from vertical semicircular canals, and 7 were classified as having convergent inputs from otoliths and canals that were spatially aligned (2 cells) or misaligned (5 cells). In addition, only 2 of 68 neurons tested responded to sinusoidal horizontal rotations in a manner typical of brainstem neurons that receive inputs from the horizontal semicircular canals. Thus, the vestibular inputs to the RVLM appear to come mainly from otolith receptors. In labyrinthectomized cats, we were unable to locate neurons with responses to tilt similar to those of cells recorded in labyrinth-intact cats, confirming that the responses attributed to vertical vestibular inputs were produced by signals from the labyrinth. In animals whose semicircular canals had been rendered dysfunctional by plugging, we only recorded responses similar to those of neurons classified as having mainly otolith inputs in canal-intact animals, indicating that the dynamic behavior of these cells does not depend upon canal inputs. The presence of otolith inputs to the RVLM is consistent with the hypothesis that this region mediates vestibulo-sympathetic reflexes involved in correcting posturally-related changes in blood pressure.

This study aimed to define the acute electrophysiological effects of the perilymphatic perfusion of streptomycin in the sensory apparatus of the semicircular canals of the frog. The ampullary DC potential, the vestibular nerve multiunit discharge, the nerve DC potential and the unitary EPSP activity were recorded in isolated semicircular canals of the frog (Rana esculenta L). The results demonstrated that perilymphatic microperfusion of streptomycin (0.1, 0.3, 1 and 3 mM) reduced both resting and mechanically evoked afferent discharge, while the response of the hair cells remains unchanged. Intracellular recordings from single afferent axons showed that the reduction of the afferent discharge was mainly due to a reduction of the amplitude, but not the frequency, of the EPSPs. These results indicate that streptomycin, when applied in the fluid bathing the synaptic pole of the sensory cells, can act as an antagonist of the vestibular afferent transmitter at the postsynaptic level.

It has been generally accepted that even in the absence of mechanical stimulation of the transductional elements, a resting depolarizing current exists which is ultimately responsible for the spontaneous release of neurotransmitter. Movement of the transductional elements modulates this resting current and thereby the evoked release of neurotransmitter occurs. Recent data from our laboratory and others have led us to question whether the relationship between spontaneous and evoked neurotransmitter release is as simple as stated. Indeed, a variety of experimental manipulations appear to influence the two modes of release differently. Examination of our results and the results of others has led us to four hypotheses: 1. the two modes of neurotransmitter release are processed differently by the hair cells; 2. cyclic AMP is involved in spontaneous but not evoked neurotransmitter release; 3. there is a positive feedback step involving an excitatory amino acid and its receptor on the hair cell in evoked neurotransmitter release and; 4. different pools of calcium are involved according to the mode of release. Accordingly, there may be several biochemical steps between the transductional movement of the stereocilia at the apex of the hair cells and the ultimate release of the neurotransmitter at the base of these cells. Some of these biochemical steps are different depending on whether the mode of release is spontaneous or evoked. These biochemical steps may amplify or at least interact with the biophysical processes previously described in the hair cells.

There are three kinds of afferent terminations in the cristae ampullares. Calyx units innervate a few neighboring type I hair cells. Bouton units contact several type II hair cells. Dimorphic units innervate both kinds of receptors. Axon diameters are largest for calyx fibers and smallest for bouton fibers. Dimorphic units supply all parts of the sensory epithelium. Calyx units are confined to the central zone of the crista and bouton units to its peripheral zone. Intra-axonal labeling was used to determine the innervation patterns of physiologically characterized afferents. Calyx units are irregularly discharging. Dimorphic units in the central zone have a more irregular discharge than those in the peripheral zone. Bouton units, which have also been identified by their slow conduction velocities, are regularly discharging. An afferent's discharge regularity, sensitivity to externally applied galvanic currents and response dynamics are more closely related to its epithelial location than to its branching pattern or to the types and number of hair cells it contacts. Of the various discharge properties studied, only the rotational gains seemed closely related to terminal morphology. Afferents innervating the central and peripheral zones differ in their innervation patterns and discharge properties. A preliminary ultrastructural study indicates that there also are regional variations in synaptic organization. Type II hair cells in the peripheral zone are contacted by many more afferent boutons than those in the central zone. Individual central boutons have multiple ribbon synapses with type II hair cells, whereas each peripheral bouton usually has a single synaptic contact. Synapses between type II hair cells and calyx endings are common centrally, but not peripherally. Two synaptic features did not vary regionally: 1) type I hair cells usually make 10-20 ribbon synapses with their calyx endings; and 2) each type II hair cell is contacted by 2-6 efferent endings. The number of efferent boutons in contact with each calyx ending declines slightly from the peripheral zone to the central zone. Reciprocal synapses were rare.

Alert cats were rotated sinusoidally (0.25 Hz) in their sagittal plane while viewing optokinetic motion in their horizontal plane. Vertical and horizontal vestibulo-ocular reflex (VOR) was measured in the dark before and after 2 h of these adaptation stimuli in upright or onside orientation of the cat. Onside exposure produced maximal adaptive horizontal VOR at the training frequency. Upright exposure produced highest gain at lower frequencies. A cat with inoperative vertical canals adapted only to upright exposure. We conclude that in the presence of horizontal image rotation either vertical canal or otolith stimulation can produce adaptation in VOR direction and stimulation of both produces complex adaptation dynamics.

Selective labyrinthine lesions were made to study the origin of excitation in the labyrinth during off-vertical axis rotation. Plugging the semicircular canals abolishes the response to rotation about a vertical axis, but optokinetic after-nystagmus (OKAN) and the sustained horizontal nystagmus induced by off-vertical axis rotation (OVAR) are maintained. After cutting the nerves of the lateral semicircular canals, neither horizontal OKAN nor the continuous horizontal nystagmus associated with off-axis rotation can be induced, although vertical OKN, OKAN and vestibular nystagmus are intact. This supports the theory that labyrinthine activity responsible for the nystagmus induced by OVAR arises in the otolith organs and couples to the oculomotor system through the velocity storage mechanism.

Responses to rotation in many vertical and horizontal planes were studied in electrically identified secondary vestibular neurons of alert cats. This report concerns secondary neurons that gave responses which could not be explained as due to a summation of semicircular canal inputs. These cells responded to sinusoidal rotation of the cat in any vertical plane, and response phase depended on the plane of rotation. The responses were modeled as the result of summation of two inputs that differed in their spatial orientations and dynamics. Response dynamics and a comparison of responses to vertical and horizontal rotations showed that some cells were sensitive to rotation with respect to gravity. Their responses both to gravity and horizontal rotations argue that these secondary neurons received convergent otolith and canal inputs. Some cells also had oculomotor related discharges and/or responded weakly to neck rotation.

We present preliminary evidence that acetylcholine has three distinct modes of action on the discharge rate of afferent fibers from the frog isolated semicircular canal. These are: (I) a facilitatory effect which is of mixed muscarinic-nicotinic type and is mediated by a receptor which we call "atropine-preferring'; (II) a suppressive effect unmasked by atropine and antagonized by strychnine whose action is mediated by a "strychnine-preferring" receptor; (III) a suppressive effect produced by the cholinesterase inhibitors eserine and echothiophate, which being antagonized by curare, is mediated by a "curare-preferring" receptor.

Hair cells isolated from the crista ampullaris of the frog (Rana pipiens) remained viable for up to 5 h and were studied using whole cell voltage- and current clamp recordings. Morphological characteristics of isolated crista hair cells were compared with hair cells studied in situ using light- and electron microscopy. While other labyrinthine hair cells such as mammalian inner and outer hair cells of the cochlea, saccular hair cells of the frog, and cochlear hair cells of the turtle typically have a cylindrical shape, the crista hair cells in the frog are predominantly bulbous, having a thin elongated trunk projecting from a spherical base just large enough to enclose the nucleus. This shape correlates well with the compressed packing configuration of hair cells of the crista ampullaris observed in situ in the histological material. The support cells often failed to separate adjacent hair cells, particularly the apical ends of the hair cells. Maximal cell density on the sensory epithelial ridge appears to be achieved by this arrangement. The mean resting membrane potential (Vz) of isolated crista hair cells was -44.8 mV. Cells with smooth surfaces and apparent opacity had the most negative Vz potentials. As the cells appeared to deteriorate, there was development of transparency and cell surface granulation. Such cells had more positive initial Vz values. Cells with Vz values more positive than -15 mV exhibited a distinct, contoured nucleus. Cells lacking these indicators of deterioration were characterized by input resistances of 1.9 +/- 0.31 G omega and membrane time constants of 13 +/- 2.5 ms. A large complex outwardly rectifying current was identified which was abolished by substituting Cs+ for K+ in the internal solution. The outward K+ current had two major components: a fast tetraethylammonium (TEA)-insensitive, voltage dependent I(A)-type current which showed voltage dependent inactivation; and a TEA sensitive current which had characteristics of a calcium dependent IK(Ca)-type current. Transient changes (20 ms duration) in membrane potential mimicking that which could be produced by the transduction current during cilial displacement potently modulated the I(A) current. Depolarizing current pulses of greater than 63800 pA were required to elicit membrane voltage oscillations. The resulting membrane potential offset of at least 40 mV is well beyond the magnitude of hair cell receptor potentials making it unlikely that these oscillations would play a role in enhancing frequency selectivity.(ABSTRACT TRUNCATED AT 400 WORDS)

The gain (slow-phase eye velocity/head velocity) of the vestibulo-ocular reflex (VOR) of 6 alert cats was sequentially adapted to values between 0.2 and 1.66 by the chronic wearing of visual reversing or 2 X magnifying spectacles, combined with forced rotation in the light. Gain was measured during sinusoidal oscillation in darkness at 0.05 Hz at a peak velocity of about 30 degrees/s. In each state of VOR gain adaptation, optokinetic nystagmus (OKN) and optokinetic afternystagmus (OKAN) were measured in a full-field optokinetic drum at velocities of 20-80 degrees/s. Steady-state, slow-phase, optokinetic eye velocity nearly equaled low drum velocities, but saturated at higher velocities and declined when drum velocity further increased. The saturation velocity varied in relation to VOR gain, ranging from 10-20 degrees/s at a VOR gain of 0.2-0.4, to 65 degrees/s at a VOR gain of 1.66. The means that the variable gain element of the VOR is shared by the optokinetic system (OKS). OKAN, measured in darkness, had a roughly exponential decay. The time constant of OKAN (Tokan) also varied with VOR gain, ranging form about 2 s at a VOR gain of 0.2, to 10 s at a VOR gain of 1.66. This is a novel finding which suggests that the velocity-storage mechanism was also affected by gain changes. A model is proposed in which a neural, variable-gain element is located in a positive-feedback, velocity-storage loop common to both the VOR and the OKS. Computer simulation showed that this hypothesis could account for most of the observed changes in OKN saturation and Tokan with changes in VOR gain. The model also predicts that low frequency VOR phase lead in darkness should increase with decreasing VOR gain. Experimental VOR phase lead at 0.05 Hz varied from about 10 degrees for VOR gains above 1.1 to about 50 degrees for VOR gains below 0.3. Such phase-lead data agree with the trend predicted by the model.

The technique of principal-component analysis was used to define anatomically the semicircular canal planes of the rhesus and squirrel monkeys with respect to the stereotaxic coordinate system. The analyses were performed on a series of points obtained from the dissected osseous labyrinths. A planar equation was defined for each canal plane in the stereotaxic coordinate system and angles were calculated between the 3 ipsilateral canal planes, between synergistic canal pairs and between each canal plane and the stereotaxic planes. The data from both species are similar: the ipsilateral canal planes are nearly orthogonal; synergistic pairs of canal planes are approximately parallel with angles of 2 degrees-12 degrees between pairs in the rhesus monkey and 13 degrees-16 degrees between pairs in the squirrel monkey. The horizontal canal planes form angles of 22 degrees and 18 degrees with the horizontal stereotaxic plane in the rhesus and squirrel monkeys, respectively. A head position of 15 degrees (pitch nose-down) was calculated to produce an optimal head position in both species for maximally stimulating the horizontal canals and minimally stimulating the vertical canals during horizontal angular acceleration. The radii of curvature (R) of the horizontal, anterior and posterior canals were also measured for both species using a calibrated reticle. These measurements indicate that the anterior canal of both species has the largest radius of curvature. This anatomical information is discussed in relation to the available physiological data.

Three series of experiments were devised to test the hypothesis that glutamate is the transmitter released by sensory hair cells of the frog semicircular canal. These three tests were: 1 - The Tolerance experiment (i.e. making the preparation tolerant to injected Glu yet still capable of responding to endogenous transmitter). 2 - The Glu Decarboxylase experiment (i.e. bathing the preparation in sufficient enzyme to prevent the effects of exogenous Glu by degrading it without affecting the response to endogenous transmitter) and; 3 - The Diltiazem experiment (i.e. using the calcium channel antagonist, diltiazem, to prevent the effect of exogenous Glu and yet not to interfere with endogenous transmitter release and action). The Tolerance and Diltiazem experiments produced results indicative of a clear dissociation between exogenous Glu and natural transmitter. The Glu decarboxylase experiment results were not so clear, producing both evidence for and against the hypothesis.

The orientation of the rat semicircular canals was determined using one of two techniques. Null point analysis was used to define physiologically the planar equations of the anterior (n = 15) and posterior canals (n = 15); equations for the horizontal canal (n = 19) were determined using an anatomical dissection technique. Canal orientation was defined with respect to stereotaxic coordinate system and, for comparison, relative to head position during freeze (startle) behavior. Results show that ipsilateral canal planes are orthogonal within 4-8 degrees, and pairs of right-left synergistic pairs are essentially co-planar. The horizontal canals are inclined upwards 35 degrees with respect to the horizontal plane, but a head position of 43 degrees nose-down was determined to produce near optimal horizontal canal and minimal vertical canal activation with horizontal rotation. Finally, a loud or unexpected auditory stimulus initiates a freeze (startle) response in rat characterized by an transient followed by a sustained head position lasting several seconds. Transients are complete within 300-400 ms. Thereafter, the head becomes momentarily stabilized in the startle position which averaged 14 +/- 8 degrees (nose-down with respect to horizontal stereotaxic zero) across the population (n = 14). The response habituated only slightly, but the final position was sufficiently variable so as to limit the usefulness of the freeze (startle) position as a reference of semicircular canal position in the rat.

The discharge activity of first-order vestibular neurons was recorded in anesthetized or decerebrated gerbils from the post-ganglionic fibers of the vestibular nerve. Semicircular canal afferents were distinguished from otolith afferents on the basis of their responses to linear and angular head acceleration. In decerebrated preparations, canal afferents exhibited significantly faster discharge activity (average = 87.8 impulses/s) than that of canal afferents in anesthetized preparations (average = 66.2 impulses/s), when the head was held to position the lateral semicircular canals coplanar with the earth horizontal plane (standard position). The effects of changes in linear forces on vestibular afferent activity were determined by statically tilting the head +/- 10 degrees about either the fore-aft and/or left-right head axes. A change in activity, from that recorded in the standard position, of 10% or greater was considered significant. Using this criterion, significant changes in the tilt response in anesthetized animals were observed in both anterior (23 of 48 neurons, 48%) and lateral (22 of 31, 71%) canal afferents as well as otolith (18 of 25, 72%) afferents. In decerebrated preparations for tilts around the pitch (left-right) axis, comparable effects were measured in (19 of 36, 53%) anterior and (17 of 30, 57%) lateral canal afferents. Neurons with irregular firing activity were more likely than regularly firing canal afferents to change their average discharge rate during static tilt. No significant differences in response magnitude to +/- 10 degrees head tilt were found between canal and otolith afferents in anesthetized animals. Mechanisms to account for the responses to linear acceleration of canal afferents are discussed.

The contribution from different pairs of semicircular canals to the generation of horizontal vestibular nystagmus was examined in monkeys. Animals with different pairs of semicircular canals surgically plugged were accelerated sinusoidally at 1 Hz (a predictive stimulus) or with steps of angular velocity (a non-predictive stimulus) about an earth vertical axis while the head was placed in various static pitch positions. In normal animals, and in animals with only the lateral canals intact, horizontal nystagmus elicited with angular velocity steps is maximal at a static pitch angle of 15 degrees nose-down (relative to the horizontal stereotaxic plane). The response follows a cosine function of the pitch angle, approaches zero at an angle of 90 degrees to the optimal orientation, and finally reverses. In animals with only the vertical canals operating, direction specific horizontal nystagmus can still be elicited. Using velocity steps, a null plane at which nystagmus reverses can be determined. It is found at about 32 degrees nose-down and thus is different from the optimal plane of the lateral canals. Consequently, it is not possible to stimulate the lateral canals maximally without stimulating the vertical canals simultaneously. Using sinusoidal rotation, nystagmus is attenuated at the static pitch position of 32 degrees nose-down, but does not reverse direction with further pitching.

A combined morphological and physiological study on the effect of saccus obliteration on the cochlea and the vestibular labyrinth of the rat is presented. Endolymphatic hydrops was successfully induced in 49% of the animals. It was frequently associated with fistulae of the membranous wall and degenerative changes in the organ of Corti and spiral ganglion. In hydropic ears electrocochleography revealed a CAP threshold increase only in those cases where hydrops was associated with loss of hair cells and ganglion cells. In two of these animals also an increased negative SP was present. Static otolith reflexes were found to be normal in all hydropic ears despite severe lesions of the saccule in some of these. Abnormal canal reflexes measured by electronystagmography and cupulometry were established in animals with hydrops of the semicircular canals and in one animal with a fistula of the saccule.

Responses to natural stimulation were studied in electrically identified secondary vestibular neurons of awake cats. A class of neurons was identified whose response dynamics and responses to rotations in several vertical and horizontal planes indicated that they received semicircular canal input. Each canal neuron had clearly defined planes of maximal and null sensitivity to rotation. The orientation of these planes indicated that 44% of the neurons received input from one pair of canals, 40% from two, and 16% from all 3 canal pairs. Many cells also had oculomotor-related discharges and/or responded weakly to neck rotation.

The response to angular acceleration of units in the superior vestibular nucleus (SVN) of barbiturate-anesthetized, cerebellectomized squirrel monkeys was used to study the distribution of semicircualr-canal inputs to the nucleus. Some so-called intact animals had 6 active semicircular canals. In other animals, the 3 canals on one side were rendered nonresponsive by plugging. In plugged animals, superior, posterior, and horizontal-canal units were encountered on both the plugged and unplugged sides, showing that all 6 canals influence the nucleus. Most units responded bilaterally to labyrinthine polarization; 92.5% of units in intact animals responded to angular acceleration, and this incidence was not decreased in plugged animals. These results suggest that most units in the superior nucleus receive bilateral canal inputs. Convergence of influences arising in orthogonally related canals was detected in less than 10% of units, so the bilateral ampullary influences must arise in parallel canals. Most SVN canal units on the plugged and unplugged sides gave type I responses, indicating that the contralateral canal influence is carried by a crossed inhibitory pathway. Most units influenced by the ipsilateral superior canal were located in the lateral half of the SVN. Posterior-canal units were in the medial half. There was no clear localization of the relatively few horizontal-canal units which were encountered.

In the present technical report, we describe a method of mechanical stimulation for single semicircular canals that is reproducible, sensitive, and discrete. The mechanical stimulator is capable of delivering reliable controlled stimuli of different waveforms over a wide frequency range that produce endolymph movements and consequent cupula deflections without motion being imparted to the animal. The results of electrophysiological experiments where the responses from pigeon (Columba livia) single horizontal semicircular canal afferent fibers produced by mechanical stimulation across a broad frequency bandwidth are reported. Comparisons between afferent fiber responses elicited by natural yaw rotation and mechanical stimulation were conducted, with the results indicating that the two stimulation methods produced responses from the same afferent unit that could be equated in magnitude. In addition, results are described from several control experiments that were conducted in order to determine the efficacy of the mechanical stimulation technique.

Sinusoidal pitch while rotating about a vertical axis in darkness causes continuous horizontal compensatory nystagmus in the monkey which persists for the duration of stimulation. The steady-state velocity sums with post-rotatory nystagmus to reduce or cancel it, suggesting involvement of the velocity storage mechanism. Analysis of the labyrinthine excitation during pitch while rotating suggests that the vertical canals play a predominant role in generating the response. Effects of selective labyrinthine lesions are in agreement with this hypothesis. Plugging the lateral canals, leaving the vertical canals intact, blocked the initial rapid response at the onset of rotation, but did not interrupt the continuous nystagmus induced by pitch while rotating. On the other hand, plugging the vertical canals abolished the response. If the lateral canal nerves were cut so that the velocity storage mechanism was inactivated, the continuous response to pitch while rotating also disappeared. The dominant labyrinth activation responsible for the nystagmus during pitching while rotating appears to arise in the vertical semicircular canals and to couple to the oculomotor system through the velocity storage mechanism.