Unilateral inner ear injury is followed by behavioral recovery due to central vestibular compensation. The therapeutic effect of oxytocin (OT) on vestibular compensation was investigated by behavioral testing in a rat model of unilateral vestibular neurectomy (UVN). Animals in the oxytocin group (UVN-OT) exhibited delayed vestibular compensation on the qualitative scale of vestibular deficits and aggravated static postural deficits (bearing surface) compared to animals in the NaCl group (UVN-NaCl). Surprisingly, oxytocin-treated animals adopt a different postural strategy than untreated animals. Instead of shifting their weight to the ipsilesional paws (left front and hind paws), they shift their weight to the front paws (right and left) without modification along the lateral axis. Furthermore, some locomotor strategies of the animals to compensate for the vestibular loss are also altered by oxytocin treatment. UVN-OT animals do not induce an increase in the distance traveled, their mean velocity is lower than that in the control group, and the ipsilesional body rotations do not increase from 7 to 30 days after UVN. This study reveals that oxytocin treatment hinders the restoration of some postural and locomotor deficits while improving others following vestibular lesions. The mechanisms of the action of oxytocin that support these behavioral changes remain to be elucidated.