The waltzing behavior is usually attributed to vestibular dysfunction. Howe
ver, the vestibular control of gaze and posture has not yet been measured q
uantitatively in any waltzing mutant. Therefore, this study was aimed at in
vestigating the relationship between inner-ear morphology, the circling beh
avior, and the vestibular control of gaze and posture in a new strain of wa
ltzing rats. Light- and electron-microscopy studies of these mutants did no
t reveal any structural abnormalities of the vestibular neural epithelia. I
n addition, the expression of Calretinin and 200-kD phosphorylated and non-
phosphorylated neurofilaments was also found to be normal in the vestibular
neural epithelia and ganglion cells. In contrast, the mutants showed sever
e dysfunctions of the vestibular control of gaze and posture. The skeletal
geometry of the alert unrestrained animals was studied using cineradiograph
y. At rest, waltzing rats held their heads tilted down: the horizontal semi
circular-canal's plane was near the earth-horizontal's plane, instead of be
ing tilted up as in Long Evans control rats. In addition, their cervical co
lumn was pitched more forward (33.6 degrees) than in the control group (6.9
degrees). The circling behavior was observed frequently, and the rats had
episodes of circling in both directions. The episodes of circling amounted
to an average of 17 turns, and the average angular velocity of the circling
was 645 degrees /s. Unilateral labyrinthectomy induced the same postural a
nd oculomotor syndromes in the waltzing and control groups. This indicates
that the mutant vestibular nerve had a significant resting discharge before
the lesion. Eye movements were recorded using acutely implanted search coi
ls. Although waltzing rats were able to perform normal spontaneous eye move
ments, they showed a complete deficit of the horizontal vestibule-ocular re
flex (HVOR) and an impairment of the maculo-ocular reflex (MOR) during cons
tant velocity, off-vertical axis rotation (OVAR). These results show, for t
he first time, that deficient transduction and/or processing of the horizon
tal-canal- and macular-related information can be causally related to the c
ircling behavior and abnormal posture, respectively.