Avian auditory and vestibular hair cells regenerate after damage by ototoxi
c drugs, but until recently there was little evidence that regenerated vest
ibular 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 large
ly 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, negati
ve-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 s
how similar recovery after hair cell regeneration. Lesions of the vestibula
r hair cells of 10-day-old chicks were created by a 5-day course of strepto
mycin sulfate. One day after completion of streptomycin treatment there was
no measurable VCR gain, and total hair cell density was similar to 35% of
that in untreated, age-matched controls. At 2 wk postlesion there was signi
ficant recovery of the VCR; at this time two subjects showed VCR gains with
in 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 VC
R 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 ce
ll regeneration, such as length of stereocilia, reafferentation of hair cel
ls, and compensation involving central neural pathways, may be involved in
behavioral recovery. Our data suggest that one or more of these factors dif
ferentially affect the recovery of these two vestibular reflexes.