'Vestibular compensation': neural plasticity and its relations to functional recovery after labyrinthine lesions in frogs and other vertebrates.

Abstract Removal of the labyrinthine organs on one side is followed by a number of severe postural and dynamic reflex deficits. Some of these deficits, in particular the posture of head and body, are normalized again over a period that varies strongly between species. Other, more persistent motor deficits are substituted, e.g. by the saccadic system. This partial normalization of the function is accompanied by changes in response properties of the central vestibular neurons on the operated side. Available evidence suggests the occurrence of reactive synaptogenesis in cat and frog. In the latter species the synaptic efficacy of commissural vestibular connections increases and the metabolic activity of central vestibular neurons on the operated side recovers post-operatively. The onset of both changes, however, is delayed by about 30 days, which is too late to be causally related with the initial, rapid period of postural recovery in frog and cat. In frogs additional, early (7–15 days p.o.) and late (45–60 p.o.) synaptic changes were detected in the brachial spinal cord. These multiple changes survive the isolation of the spinal cord and must be propriospinal in origin. Selective lesions of individual vestibular nerve branches indicate that inactivation of utricular inputs is a sufficient and necessary condition to provoke postural deficits and early spinal changes similar to those after hemilabyrinthectomy. Therefore, a close correlation between spinal plasticity and postural recovery is indicated. In essence, the elimination of vestibular afferent inputs results in a series of behavioral distortions that are partially normalized by a multitude of synaptic mechanisms at distributed anatomical sites over different periods of time.