Head tilt in rats during exposure to a high magnetic field.

During exposure to high strength static magnetic fields, humans report vestibular symptoms such as vertigo, apparent motion, and nausea. Rodents also show signs of vestibular perturbation after magnetic field exposure at 7 tesla (T) and above, such as locomotor circling, activation of vestibular nuclei, and acquisition of conditioned taste aversions. We hypothesized that the acute effects of the magnetic field might be seen as changes in head position during exposure within the magnet. Using a yoked restraint tube that allowed movement of the head and neck, we found that rats showed an immediate and persistent deviation of the head during exposure to a static 14.1 T magnetic field. The direction of the head tilt was dependent on the orientation of the rat in the magnetic field (B), such that rats oriented head-up (snout towards B+) showed a rightward tilt of the head, while rats oriented head-down (snout towards B-) showed a leftward tilt of the head. The tilt of the head during magnet exposure was opposite to the direction of locomotor circling immediately after exposure observed previously. Rats exposed in the yoked restraint tube showed significantly more locomotor circling compared to rats exposed with the head restrained. There was little difference in CTA magnitude or extinction rate, however. The deviation of the head was seen when the rats were motionless within the homogenous static field; movement through the field or exposure to the steep gradients of the field was not necessary to elicit the apparent vestibulo-collic reflex.

Mobile telephone use effects on peripheral audiovestibular function: a case-control study.

Low level radio-frequency (RF) signals may produce disorientation, headache and nausea. This double blind study tested nine case-subjects, who complained of various symptoms after prolonged mobile telephone use and 21 control subjects. Each subject underwent a series of trials, in which a dummy mobile telephone exposure system was held to each ear for 30 min in (a) pulsed, (b) continuous RF emission or, (c) no emission test modes. In the active pulsed and continuous modes the same mean power as the output of a typical handset was delivered at a carrier frequency of 882 MHz and at a maximum specific absorption rate (SAR) value of 1.3 W kg(-1) (+/- 30%). In Experiment I (auditory), transient evoked otoacoustic emissions (TEOAE), which assess the outer hair cells in the inner ear, were conducted. In Experiment II (vestibular) the vestibulo-ocular reflex was recorded by video-oculography (VOG), at baseline and immediately post exposure. There were no significant TEOAE changes from baseline to post-exposure recording for any of the exposures and no significant differences in the TEOAEs' change from baseline to post exposure between cases and controls. The VOG did not identify any effect of the exposure on the vestibular end organ in either cases or controls. In conclusion, 30 min exposure to mobile phone RF did not show any immediate effects on vestibulocochlear function as measured by TEOAE and the VOR.

Memory trace of motor learning shifts transsynaptically from cerebellar cortex to nuclei for consolidation.

Adaptation of ocular reflexes is a prototype of motor learning. While the cerebellum is acknowledged as the critical site for motor learning, the functional differences between the cerebellar cortex and nuclei in motor memory formation are not precisely known. Two different views are proposed: one that the memory is formed within the cerebellar flocculus, and the other that the memory is formed within vestibular nuclei. Here we developed a new paradigm of long-term adaptation of mouse horizontal optokinetic response eye movements and examined the location of its memory trace. We also tested the role of flocculus and inferior olive in long-term adaptation by chronic lesion experiments. Reversible bilateral flocculus shutdown with local application of 0.5 microl-5% lidocaine extinguished the memory trace of day-long adaptation, while it very little affected the memory trace of week-long adaptation. The responsiveness of vestibular nuclei after week-long adaptation was examined by measuring the extracellular field responses to the electrical stimulation of vestibular nerve under trichloroacetaldehyde anesthesia. The amplitudes and slopes of evoked monosynaptic field response (N1) of week-long adapted mice were enhanced around the medial vestibular nucleus compared with those of control mice. Chronic flocculus or inferior olive lesions abolished both day and week-long adaptations. These results suggest that the functional memory trace of short-term adaptation is formed initially within the cerebellar cortex, and later transferred to vestibular nuclei to be consolidated to a long-term memory. Both day and week-long adaptations were markedly depressed when neural nitric oxide was pharmacologically blocked locally and when neuronal nitric oxide synthase was ablated by gene knockout, suggesting that cerebellar long-term depression underlies both acquisition and consolidation of motor memory.

Galvanic vestibular stimulation modifies vection paths in healthy subjects.

The present study aimed at determining whether vestibular inputs contribute to the perception of the direction of self-motion. This question was approached by investigating the effects of binaural bipolar galvanic vestibular stimulation (GVS) on visually induced self-motion (i.e., vection) in healthy subjects. Stationary seated subjects were submitted to optokinetic stimulation inducing either forward or upward linear vection. While perceiving vection, they were administered trapezoidal GVS of different intensities and ramp durations. Subjects indicated the shape and direction of their perceived self-motion path throughout the experiment by a joystick, and after each trial by the manipulation of a 3D mannequin. Results show that: 1) GVS induced alterations of the path of vection; 2) these alterations occurred more often after GVS onset than after GVS offset; 3) the occurrence of vection path alterations after GVS onset depended on the intensity of GVS but not on the steepness of the GVS variation; 4) the vection path deviated laterally according to either an oblique or a curved path; and 5) the vection path deviated toward the cathode side after GVS onset. It is the first time that vestibular information, already known to contribute to the induction of vection, is shown to modify self-motion perception during the course of vection.

Electrical activation of the human vestibulo-sympathetic reflex.

Muscle sympathetic nerve activity (MSNA) is modulated on a beat-to-beat basis by the baroreflex. Vestibular input from the otolith organs also modulates MSNA, but characteristics of the vestibulo-sympathetic reflex (VSR) are largely unknown. The purpose of this study was to elicit the VSR with electrical stimulation to estimate its latency in generating MSNA. The vestibular nerves of seven subjects were stimulated across the mastoids with short trains of high frequency, constant current pulses. Pulse trains were delivered every fourth heartbeat at delays of 300-700 ms after the R wave of the electrocardiogram. Vestibular nerve stimulation given 500 ms after the R wave significantly increased baroreflex-driven MSNA, as well as the diastolic blood pressure threshold at which bursts of MSNA occurred. These changes were specific to beats in which vestibular stimulation was applied. Electrical stimulation across the shoulders provided a control condition. When trans-shoulder trials were subtracted from trials with vestibular nerve stimulation, eliminating the background baroreflex-driven sympathetic activity, there was a sharp increase in MSNA beginning 660 ms after the vestibular nerve stimulus and lasting for about 60 ms. The increase in the MSNA produced by vestibular nerve stimulation, and the associated increase in the diastolic blood pressure threshold at which the baroreflex-driven bursts occurred, provide evidence for the presence of a short-latency VSR in humans that is likely to be important for the maintenance of blood pressure during rapid changes in head and body position with respect to gravity.

Vestibulo-collic reflex (VCR) in mice.

The vestibulo-collic reflex (VCR) attempts to stabilize head position in space during motion of the body. Similar to the better-studied vestibulo-ocular reflex, the VCR is subserved by relatively direct, as well as indirect pathways linking vestibular nerve activity to cervical motor neurons. We measured the VCR using an electromagnetic technique often employed to measure eye movements; we attached a loop of wire (head coil) to an animal's head using an adhesive; then the animal was gently restrained with its head free to move within an electromagnetic field, and was subjected to sinusoidal (0.5-3 Hz) or abrupt angular acceleration (peak velocity approximately 200 degrees/s). Head rotation opposite in direction to body rotation was assumed to be driven by the VCR. To confirm that the compensatory head movements were in fact vestibular in origin, we plugged the horizontal canal unilaterally and then retested the animals 2, 8 and 15 days after the lesion. Two days after surgery, the putative VCR was almost absent in response to abrupt or sinusoidal rotations. Recovery commenced by day 8 and was nearly complete by day 15. We conclude that the compensatory head movements are vestibular in origin produced by the VCR. Similar to other species, there are robust compensatory mechanisms that restore the VCR following peripheral lesions.

Dynamics and directionality of the vestibulo-collic reflex (VCR) in mice.

The vestibulo-collic reflex (VCR) stabilizes the head in space by excitation of neck muscles that oppose head rotation. Recently, the mouse vestibulo-ocular reflex (VOR) has been characterized so that genetic manipulations of the vestibular system can be examined. We have characterized the dynamics and directionality of the VCR in mice restrained at the neck so that studies of vestibular system genetics may include comparisons to normal VCR in addition to VOR. Head rotations were measured in darkness with a three-dimensional search coil system during whole body rotations. The VCR in four C57BL/6 mice was present in pitch, roll, and yaw directions with an overall average gain of 0.28. Phase was accurately compensatory to oppose head rotation across a wide range of frequencies from 0.02 Hz to 2.0 Hz. Compensatory head rotations were greatest in the direction opposing the applied stimulus and weak or absent in other directions. Constant velocity rotations about horizontal axes elicited head velocity modulation and bias similar to that observed in the VOR. We conclude that the VCR of mice is similar to that in other mammals.

Visual influences on the development and recovery of the vestibuloocular reflex in the chicken.

Whenever the head turns, the vestibuloocular reflex (VOR) produces compensatory eye movements to help stabilize the image of the visual world on the retina. Uncompensated slip of the visual world across the retina results in a gradual change in VOR gain to minimize the image motion. VOR gain changes naturally during normal development and during recovery from neuronal damage. We ask here whether visual slip is necessary for the development of the chicken VOR (as in other species) and whether it is required for the recovery of the VOR after hair cell loss and regeneration. In the first experiment, chickens were reared under stroboscopic illumination, which eliminated visual slip. The horizontal and vertical VORs (h- and vVORs) were measured at different ages and compared with those of chickens reared in normal light. Strobe-rearing prevented the normal development of both h- and vVORs. After 8 wk of strobe-rearing, 3 days of exposure to normal light caused the VORs to recover partially but not to normal values. In the second experiment, 1-wk-old chicks were treated with streptomycin, which destroys most vestibular hair cells and reduces hVOR gain to zero. In birds, vestibular hair cells regenerate so that after 8 wk in normal illumination they appear normal and hVOR gain returns to values that are normal for birds of that age. The treated birds in this study recovered in either normal or stroboscopic illumination. Their hVOR and vVOR and vestibulocollic reflexes (VCR) were measured and compared with those of untreated, age-matched controls at 8 wk posthatch, when hair cell regeneration is known to be complete. As in previous studies, the gain of the VOR decreased immediately to zero after streptomycin treatment. After 8 wk of recovery under normal light, the hVOR was normal, but vVOR gain was less than normal. After 8 wk of recovery under stroboscopic illumination, hVOR gain was less than normal at all frequencies. VCR recovery was not affected by the strobe environment. When streptomycin-treated, strobe-recovered birds were then placed in normal light for 2 days, hVOR gain returned to normal. Taken together, the results of these experiments suggest that continuous visual feedback can adjust VOR gain. In the absence of appropriate visual stimuli, however, there is a default VOR gain and phase to which birds recover or revert, regardless of age. Thus an 8-wk-old chicken raised in a strobe environment from hatch would have the same gain as a streptomycin-treated chicken that recovers in a strobe environment.

The influence of light on modulation of the human vestibulo-ocular reflex.

The goal of this study was to investigate the influence of light, without retinal slip information, on the ability to generate eye movements to compensate for head rotations. Subjects were rotated sinusoidally at 1.0, 2.0 or 3.0 Hz at a peak velocity of 30 deg/sec while they: 1) performed mental arithmetic in darkness; 2) attempted to view the remembered location of a stationary target in darkness; 3) attempted to view the remembered location of the stationary target through translucent contact lenses that allowed the passage of light but did not provide any target information (ganzfeld stimulus); 4) directly viewed the illuminated stationary target. The gain of compensatory eye movements was least while subjects viewed through the translucent contact lenses (median = 0.76), intermediate while subjects either performed mental arithmetic in darkness (median = 0.84) or attempted to view the remembered location of the target in darkness (median = 0.84), and greatest if they actually viewed the target (median = 0.95). Our findings suggest that factors other than light alone account for the increased gain of compensatory eye movements that occurs when subjects view rather than imagine a stationary target.

Subdural application of hemoglobin to the cerebellum blocks vestibuloocular reflex adaptation.

Vestibuloocular reflex (VOR) was induced by horizontal sinusoidal whole-body rotation in darkness in rabbits and a monkey. One eye was observed through an infrared TV camera. The gain of VOR was adaptively changed when the animal was continuously rotated for 3 h with the observed eye exposed to the screen moving in phase or out of phase with the head. Injection of 0.1 ml saline solution containing 10 microM hemoglobin into the subdural space over the cerebellar flocculus ipsilateral to the observed eye abolished the VOR adaptation. Since hemoglobin absorbs nitric oxide, which mediates synaptic plasticity in the cerebellar cortex, these results support the view that synaptic plasticity of the flocculus plays a key role in the VOR adaptation.