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.

Recovery of the vestibulocolic reflex after aminoglycoside ototoxicity in domestic chickens.

Avian auditory and vestibular hair cells regenerate after damage by ototoxic drugs, but until recently there was little evidence that regenerated vestibular hair cells function normally. In an earlier study we showed that the vestibuloocular reflex (VOR) is eliminated with aminoglycoside antibiotic treatment and recovers as hair cells regenerate. The VOR, which stabilizes the eye in the head, is an open-loop system that is thought to depend largely on regularly firing afferents. Recovery of the VOR is highly correlated with the regeneration of type I hair cells. In contrast, the vestibulocolic reflex (VCR), which stabilizes the head in space, is a closed-loop, negative-feedback system that seems to depend more on irregularly firing afferent input and is thought to be subserved by different circuitry than the VOR. We examined whether this different reflex also of vestibular origin would show similar recovery after hair cell regeneration. Lesions of the vestibular hair cells of 10-day-old chicks were created by a 5-day course of streptomycin sulfate. One day after completion of streptomycin treatment there was no measurable VCR gain, and total hair cell density was approximately 35% of that in untreated, age-matched controls. At 2 wk postlesion there was significant recovery of the VCR; at this time two subjects showed VCR gains within the range of control chicks. At 3 wk postlesion all subjects showed VCR gains and phase shifts within the normal range. These data show that the VCR recovers before the VOR. Unlike VOR gain, recovering VCR gain correlates equally well with the density of regenerating type I and type II vestibular hair cells, except at high frequencies. Several factors other than hair cell regeneration, such as length of stereocilia, reafferentation of hair cells, and compensation involving central neural pathways, may be involved in behavioral recovery. Our data suggest that one or more of these factors differentially affect the recovery of these two vestibular reflexes.

Intraventricular infusion of arginine vasotocin induces singing in a female songbird.

Arginine vasotocin (AVT) has been implicated in the activation of courtship and aggressive behaviors in many vertebrate taxa. Here, we tested its effect on singing and other vocal behavior in a songbird. Female white-crowned sparrows (Z. l. gambelii) were implanted with chronic cannulae aimed at the third ventricle. Infusions of AVT dramatically increased the number of songs and other vocalizations during a 40 min period following infusion. Half of the subjects sang full song following AVT treatment. No bird sang after treatment with saline; any type of vocalization after saline treatment was rare. Female white-crowned sparrows are known to sing in both spring and winter in the wild; this behavior is thought to be aggressive, functioning in dominance interactions and territoriality. Central infusion of AVT induced singing and other vocalizations in estrogen-primed, photostimulated subjects as well as in non-reproductive subjects housed on short photoperiods. Thus, the effects of AVT on vocal behavior may not require breeding levels of gonadal steroids and are probably not seasonal. We hypothesize that both in the breeding and non-breeding seasons, AVT increases motivation to sing.

The startle eyeblink response to low intensity acoustic stimuli.

Four experiments were conducted to investigate the acoustic startle response to stimuli of low intensities. Eyeblink responses (integrated EMG from orbicularis oculi) were measured from male and female college students. Experiment 1 compared tone and noise stimuli varying in intensity (50 and 60 dB(A) SPL), with noise stimuli producing greater response amplitude and probability than tone stimuli. Experiment 2 was designed to investigate temporal summation of low intensity stimuli using single and paired 70dB(A) SPL broadband noises, and an onset-to-onset interval between the brief stimuli in a pair equal to the duration of the single stimuli. Increasing the duration of single stimuli resulted in larger responses, illustrating temporal summation. Experiment 3 used 60 and 70 dB(A) SPL broadband noise varying in rise/fall time, with faster-rising stimuli producing larger responses, and more intense stimuli producing larger and more probable responding. Experiment 4 employed the startle modification paradigm using 60 and 70 dB(A) SPL broadband noises as startle stimuli and a 50dB(A) SPL tone as a prepulse. Response amplitude and probability to both 60 and 70 dB(A) SPL stimuli were significantly inhibited by the 50dB(A) SPL prepulse. These studies show that the acoustic startle response is more sensitive than previously thought, and the elicitation of startle by low intensity stimuli argues against the limitation of the startle reflex as a high intensity phenomenon. These findings can increase the application of this response system by showing that startle stimuli need not be of high intensity, because reliable and differential startle can be elicited and modified at relatively low stimulus intensities.